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  Topic: bFast's Allele Blender, Zachriel< Next Oldest | Next Newest >  
Zachriel



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(Permalink) Posted: Mar. 08 2008,21:55   

bFast proposes a simulation.
Quote
bFast: 1111111222 2212112211 1221212112 1112222121 1212221112 1112212112 1112122121 1122212212 1221122222 1121121121 2221122222 2221112122 1121121112 2221222212 1222211212 1221212121 1221111221 1122121111 1122212112 1212112222
SUM = 301

Bob O'H: you’re illustrating a well known problem, genetic drift. With a population size of 5, the relative fitness has to be very large to have a visible effect. Drift is a large factor in small populations, so even alleles which reduce fitness can become fixed.

Bob O'H makes an important point. Some alleles will become fixed even without selection.

Meanwhile, in a reasonable population of competitors, their overall fitness will tend to improve. That inevitably means more and more individual alleles will improve, even if particular alleles are gained or lost along the way.

This is an example of how global pressure can bring about local changes.


--
Update: The results are much as expected. In a recent run, I used a 100x100 grid for a population of 10000. Each genome is 100. When a replication occurs, there is a 10% chance of a mutation. Only 1's and 2's are allowed thus far. The child then displaces a weaker neighbor, if any. This creates a nice nested distribution of varieties across the grid. After 100 generations, the average fitness is about 1.8 per allele. The corners of the grid tend to have more primitive varieties. This is a typical genome:

1212112211 2122222212 2222212222 2222222221 2122222221
2212222122 2122122211 1222221212 1222222112 2122222222

Next step is to allow very rare 2-to-3 mutations. I'm also considering some sort of sexual recombination, but watching 1's doin' it doesn't strike me as particularly interesting.

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Zachriel



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(Permalink) Posted: Mar. 08 2008,21:58   

Quote (Zachriel @ Mar. 07 2008,06:47)
bFast proposes a simulation.
Quote
bFast: 1111111222 2212112211 1221212112 1112222121 1212221112 1112212112 1112122121 1122212212 1221122222 1121121121 2221122222 2221112122 1121121112 2221222212 1222211212 1221212121 1221111221 1122121111 1122212112 1212112222
SUM = 301

Allele Blender uses a typical selection criteria called The Early Bird Gets the Worm, also known as I only need to outrun you, Albert. In other words, strong positive selection. Lately, I've allowed very rare 2-to-3 mutations. Of course, while some are lost, once established they tend to quickly dominate the population.

I have tried to contact bFast to make sure I have represented his model correctly. The only contact I have found is at ISCID. Someone might want to give bFast a heads up.

* Niels Bohr and Albert Einstein were taking a walk in the woods, vigorously debating the philosophical underpinnings of quantum theory, when a gigantic bear suddenly burst out of the underbrush and raced toward them. Niels immediately whipped out his fine running shoes and began lacing them up.

Einstein, furrowing his brow at Bohr, said: "Niels, there's no way you can outrun that bear."

"That's true," Bohr calmly replied, "but I don't need to outrun the bear. I only need to outrun
you, Albert."


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Zachriel



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(Permalink) Posted: Mar. 08 2008,21:59   

Quote (Zachriel @ Mar. 07 2008,06:47)
bFast proposes a simulation.
Quote
bFast: 1111111222 2212112211 1221212112 1112222121 1212221112 1112212112 1112122121 1122212212 1221122222 1121121121 2221122222 2221112122 1121121112 2221222212 1222211212 1221212121 1221111221 1122121111 1122212112 1212112222
SUM = 301

These are all adjustable, of course:
* Alleles can now vary from 1 to 9.
* Mutations occur every 10% of replications.
* Only 10% of these 10% can cause an incremental improvement, most of the rest being detrimental.

Fitness rapidly improves.
Recombination with a random neighbor improves even faster.
Recombination with the fittest available neighbor is faster still.

But recombination with the most attractive neighbor still works very well, but has a peculiar effect. To simulate this, the Peahen chooses a mate from the immediate neighborhood—not based on fitness—but based on the one with the prettiest tail. The prettiest tail is defined as the longest length of trailing 1's—a trait which is actually detrimental to the overall fitness.

The Peacocks Tail



Notice the family resemblance among neighbors, and the small clan of uglies in the middle left column. This run has a genome of length twenty so you can more easily see the effect.



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Zachriel



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(Permalink) Posted: Mar. 08 2008,22:19   

Quote (bFast @ Mar. 08 2008,19:18)
I have written my own sim at this point, and it fails miserably!  So bad, in fact, that I think it must have a bug.

It isn't necessary to reinvent the wheel. I believe I have a working simulator. It's open source, and I'm more than willing to share. However, I want to make sure that the model correctly represents what you are trying to test.

We have a population, each member represented by a genome. Each allele is a numeral. A member spawns a Child which then competes in the population. Fitness is determined by the sum of genes.

In the Allele Blender, each member of the population is located on a grid. Each new Child will replace the weakest in the vicinity, assuming the Child is fitter. Is this correct?

(By the way, starting with your original organisms, and assuming strong positive selection, Organism 2 will quickly dominate the population. The 3-allele in Organism 4 will almost definitely be lost.)

Quote (bFast @ Mar. 08 2008,19:18)
- No new alleles are created during the simulation.  I suspect that the addition of new alleles would increase the noise, therefore increasing the problem.

I assume you mean more than two available versions at each locus. Using your concept, it was easy to have nine varieties, 1 through 9. If a given gene is a 2, then a standard mutation as described above would be either a 1 (detrimental) or a 2 (neutral). Very occasionally we might see a 2 increment to a 3. A novelty.

Quote (bFast @ Mar. 08 2008,19:18)
- The number of alleles per organism is small (initially 200).  I suspect that the more alleles, the worse the signal to noise problem.

I think you mean the number of genes (each allele being represented by a numeral). It's just a parameter. I can adjust that to any reasonable number. There are several relationships that we can discover that will help us extrapolate to larger numbers. I'll provide some details later.

Quote (bFast @ Mar. 08 2008,19:18)
Selection is, well "pure", the definition of "fit" never changes, every organism death is determined by its ideally measured fitness compared to another organism.  This is a very positivistic model.

That seemed to be your intent. But that can be easily adjusted. I have already added proximity, recombination, random mate selection, mate selection for fitness, and mate selection for an arbitrary trait (the peacock's tail). We could also add a random fudge factor. It doesn't really change the end result. Even with no selection, alleles become fixed. It's an important concept that I would be happy to discuss.

       ' Recombine
       For a = 1 To numAllele
           If Rnd < 0.5 Then
               Mid(Child, a, 1) = Mid(Mate, a, 1)
           Else
               Mid(Child, a, 1) = Mid(Parent, a, 1)
           End If
       Next a


Quote (bFast @ Mar. 08 2008,19:18)
I would love to hammer this challenge out with you to prove that in an ideal world a new mutation actually can catch on.  I would also love to see the sim prove that a mutation is more likely to fix in a large population.  So far my sim isn't doing any better with a large population (its a dog by about 50,000).

Not only can new mutations fix, but they can do so in the absence of selection.

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Zachriel



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(Permalink) Posted: Mar. 08 2008,22:19   

Quote (bFast @ Mar. 08 2008,19:18)
I would love to hammer this challenge out with you to prove that in an ideal world a new mutation actually can catch on.  

Hi bFast! I have several open source projects that demonstrate various aspects of evolution.

Nest of Letters shows how even neutral mutations can and will become fixated in populations.



Killer Rabbits started with a very cool simulation by Wonders for Oyarsa posted on Telic Thoughts. Ironically, he overlooked the process of fixation that was staring him in the face.



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Zachriel



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(Permalink) Posted: Mar. 09 2008,08:17   

Neutral Drift and the Law of Small Numbers

Consider a single locus in a population limited by circumstance to just two.

       A, B

Let them replicate.

       A1, A2, B1, B2

Now, we keep two at random. These are the possibilities.

       A1, A2
       A1, B1
       A1, B2
       A2, B1
       A2, B2
       B1, B2


There is a one in three chance of forever losing one of the two alleles. But let's assume that we end up with both alleles. But then, over each succeeding generation, we are again faced with a one in three chance of forever losing one of the two alleles. Sooner or later, we will have A, A or B, B. Fixation.

Now consider a population of three.

       A, B, C

Replicate.

       A1, A2, B1, B2, C1, C2

Now choose three. There are twenty possibilities. Some of them include all three alleles. But some don't. Even if all three alleles make it into the next generation, we are again faced with a significant possibility of losing one of the alleles forever. Eventually, we will lose one allele. Such as this.

       A, A, B

Now replicate

       A1, A2, A3, A4, B1, B2

Again, choose three. Notice that there is a finite chance of keeping both alleles. But there is also a finite chance of losing another allele forever. Eventually, this will happen. Fixation.

Which allele will become fixed? It's random. So in the first case, it is 1/2. In the second case, it is 1/3. But notice that it takes longer with the larger population. Indeed, Hardy-Weinberg proved that in an infinite (undisturbed) population, the rate of fixation is zero. But no population is infinite.

But we can make an even more powerful statement. Instead of a single allele, consider a genome of a 100 alleles. Assume, the rate of neutral mutation is 1 per 100 per allele per replication. That means each genome will have a single mutation. If it replicates a hundred children, then the average locus will have experienced one mutation (an average of one per child). What is the chance of a particular allele being fixed? One in a hundred. So what is the Expected Number of some mutation becoming fixed when we have a hundred mutations? 100*1/100 = 1. It's the same for any size genome, any size population. The rate of fixation of neutral mutations is equal to the rate of neutral mutations regardless of population size.

This is not an empirical result. It's arithmetic, and is based on the assumption of neutrality. From what I gather, you are attempting to understand the case of nearly neutral evolution.

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Zachriel



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(Permalink) Posted: Mar. 09 2008,08:43   

In any case, you haven't provided us enough information to be sure we are properly simulating your model.  If we consider these two genomes:

       1111111111111111111...

and

       1111121111111111111...

You've defined fitness as the sum of the alleles. Assuming strong positive selection and a low mutation rate, the 2-mutation should quickly dominate the population. With a high mutation rate, then various mutants will compete to dominate the population, but any pure-strain will be quickly overwhelmed.

Among your original organisms, Organism 2 will quickly dominate the population. The 3-allele in Organism 4 will almost definitely be lost. But then any future advantageous mutation to the dominant Organism 2 will then come to dominate the population:

       xxxxxxxxxxxxxxxxxxxxxx...

and

       xxxxxXxxxxxxxxxxxxxxxx...

Remember, Neils only has to outrun Albert.

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Zachriel



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(Permalink) Posted: Mar. 09 2008,09:41   

Quote (Zachriel @ Mar. 08 2008,22:19)
I have already added proximity, recombination, random mate selection, mate selection for fitness, and mate selection for an arbitrary trait (the peacock's tail).

I changed sexual selection for the tail to be a preference for a long tapering tail.

I am allowing the 'head', the two leading loci, to mutate faster. This results in faster evolution in that region. (I'll probably fiddle with that feature. Maybe allow the head region to expand.) Here's a typical organism.

      99544535322222111111

Notice the 'head' has hit the limit of 99. The tail is ...322222111111, but you can guess that some of its relatives probably have longer tails. (They do.) It's quite amazing how powerful sexual selection for an arbitrary trait can be at shaping the organism.


Update

Took out the 'head'. Too contrived.

Trying longer genomes. Works as before, with or without recombination, with or without mating selection for fitness, with or without mating selection for a beautiful tail.

  ' Beauty is in the eye of the beholder
  ' Long tapering tails preferred


  Public Function calcBeauty(Mate) As Integer
  Dim mv, mk As Integer
 
      mk = Val(Right(Mate, 1))
      calcBeauty = 0
 
      For a = numGenes To 1 Step -1
          mv = Val(Mid(Mate, a, 1))
          If mv = mk Or mv = mk + 1 Then
              calcBeauty = calcBeauty + 10 \ (mv + 1)
' Thinner the better
              mk = mv
          Else
              Exit For
          End If
      Next a

  End Function


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Zachriel



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(Permalink) Posted: Mar. 09 2008,10:14   

bFast emailed and said he has his simulator working. However, his email didn't reveal details sufficient to replicate his results. Unsurprisingly, he does say it confirms his suspicions.

bFast, when you get the chance, maybe you could provide some examples using small genomes and populations so we can see how it works. Then it should be easy to scale it up once we understand what you are modeling.

My first question has nothing with introducing the novel 3-allele mutation: Why doesn't Organism 2 quickly dominate the population? Why would you think that Organism 4 with the 3-allele would propogate? I would expect that line to die out and be replaced by Organism 2. Indeed, without new mutations being introduced, we would expect the entire population to be dominated by clones of Organism 2. Organism 4's only hope is to find a rock to hide under.

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Annyday



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(Permalink) Posted: Mar. 09 2008,14:54   

I am not in the least bit a programmer, but if you're actually getting funky results from a simulation, bFast, I'd like to see the simulator and the results. Mathematical modeling of changing populations is a mainstay of evolutionary theory, so funky results in simulations are pretty interesting.

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bFast



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(Permalink) Posted: Mar. 09 2008,18:06   

The question that I present is, how easy is it for natural selection to favor an advantageous point mutation (signal) in light of the various destractions (noise)?

I see noise in four areas:

1 - Allele populations.  Organisms, such as myself, consist of a mishmash of alleles that exist within the community of origin.  As such, any one individual will not have an ideal mix of alleles.  If an organism, such as myself, has the lucky slightly beneficial point mutation, will natural selection be able to favor it dispite all of the other alleles flying around in the population.

2 - New alleles.  Each individual organism will be hit with zero to a few mutations within the active DNA.  The fact that each organism is de-idealized by these mutations increases the noise, making it more difficult for natural selection to be able to favor a slightly beneficial point mutation.

3 - The fickleness of natural selection.  In two given contexts natural selection will favor different alleles.  For instance, I am more intelligent than most.  As such, I have a good allele set wrt intelligence.  I am decidedly less athletic than most.  As such, I don't have a good allele set wrt athletics.  If a given opportunity for selection involves me and a friend trying to outrun a hungry bear, in all likelihood my above average intelligence will do me no good, and I'll be lunch.  To make matters worse, I think that natural selection is probably best at ignoring allele mixes altogether, and causing one to be removed from the pool for no reason other than being in the wrong place at the wrong time.

4 - Bulk-editing.  Alleles come with an entire gene full of baggage.  Our dear lucky mutation has to happen within an existing allele.  This existing allele may not be a rising star.  Now a new allele exists which may be marginally better than its falling star cousin, but may not be sufficiently advantageous to beat out other alleles floating around in the population.  When organisms such as myself produce offspring, we generally exchange genetic data in bulk units called chromosomes.  So even if a gene is a particularly good one, I think that the fact that it is packaged up in a chromosome presents a challenge.

Now, I have produced a simulation that selects out issue number 1.  The question is, is noise source 1 in itself sufficient to disable natural selection for a slightly beneficial mutation?

My sim's algorithm is as follows:

Initialization accepts 3 parameters: gene count, population, mutant count.

- Per population, I create an organism
-   Per organism, I create an array of 'gene count' elements.
-   Each element is initialized with a random 0 or 1, representing allele #0 or allele #1 where we assume that the #1 allele is 'fitter' than #0.
-   Each element is given a 'fitness' number -- the total of 1's in its genes.
-   for 'mutant count', organisms are selected at random, and the first gene is boosted to allele #2.  The 'fitness' number is adjusted.

Processing accepts 1 parameter: cycles and returns the total number of active mutants.

- Per cycle:
-    two organisms are selected at random
-    the less fit of the two is decomissioned, and replaced by:
-       two organisms are selected at random
-       through the genes of these organisms, either the first or 2nd organism's allele will be selected.
- the 'fitness' of the new organism is measured.

One "generation" is considered to be Population cycles (on average, the death/replacement of each individual.)

The general results of my sim are as follows (I haven't run lots of simulations yet, nor have I done careful logging yet.):

- when there are 200 alleles per organism, the mutant dies very about 9 times out of 10.  If the mutant lives to get about 20 organisms to contain it, it rather quickly becomes fixed.  Dying or fixing doesn't seem to have much to do with population.

- when there are 2000 alleles per organism, the mutant dies rather often, often enought that I have skipped past early processing and seeded the system with multiple mutants.  If it has 50 mutants in a 1000 population, the mutant usually survives, and fixes rather quickly.

- when there are 20,000 alleles per organism, the population of the mutant seems to wander like it is influenced by the throwing of a dice -- genetic drift.  I have been seeding with 100 in a population of 1000, and have yet to be able to get it to fix.  

NOTE: As all allele 1s are motivated to increase in popularity, one may consider that a bunch of them have fixed within this process.  As they fix, the amount of noise, the number of alleles in the population decreases.  I have not yet measured the number of fixed alleles in the calculation, but I suspect that with the small counts, the reason NS grabs the beneficial mutation so solidly at some point is because the noise has significantly decreased.

Now, in real world organisms, there is (almost) always an abundance of available alleles.  In fact, when there are not, it is conserning.  This is caused, of course, by other organisms obtaining mutants that have infiltrated the population.  Populations always have many alleles, so the mutant of interest fixing because all of the nearby alleles fixing is an artificial situation.

A major question that I have as I present this sim is, how many alleles are there in a population.  I could envision that there are a whole lot.  I know that I contain 2 sets of genes, each set has 25,000 coding genes.  My wife also has 2 sets of genes.  So between the two of us, let alone our neighbors, we have 100,000 coding genes.  But, for how many of those genes is there only one allele within the population?  For how many of those genes are there literlally hundreds of alleles?  Bottom line, how many alleles are disguising my lucky beneficial mutation.  My sim suggests that somewhere less than 20,000 is too many, that it produces too much noise for natural selection to filter out, when selecting a beneficial point mutation -- and that, dispite the other sources of noise as described above.

  
bFast



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(Permalink) Posted: Mar. 09 2008,19:00   

Zachriel, "Indeed, without new mutations being introduced, we would expect the entire population to be dominated by clones of Organism 2. Organism 4's only hope is to find a rock to hide under."

In an asexual environment, this would obviously be so.  Which presents a problem.  It would seem that in an asexual environment, the signal to noise issue becomes very much stronger.  It is only in the most fit of organisms, that an advantageous mutation would stand a breath of a chance.   ???

  
Zachriel



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(Permalink) Posted: Mar. 09 2008,21:31   

Quote (bFast @ Mar. 09 2008,18:06)
- Per cycle:
-    two organisms are selected at random
-    the less fit of the two is decomissioned, and replaced by:
-       two organisms are selected at random
-       through the genes of these organisms, either the first or 2nd organism's allele will be selected.
- the 'fitness' of the new organism is measured.

That's a rather odd selection method. You pit organism 1 against organism 2, but it's not the victor that reproduces, but a recombination of two other organisms. I suppose it should result in evolution towards higher fitness, though. I'll test it to be sure.

Quote (bFast @ Mar. 09 2008,18:06)
- when there are 200 alleles per organism, the mutant dies very about 9 times out of 10.

Yes, of course.

That's what we would expect for a near neutral mutation (your mutation only increases fitness by a small percentage) in the midst of chaos (randomized genomes). So?

Quote (bFast @ Mar. 09 2008,18:06)
As all allele 1s are motivated to increase in popularity, one may consider that a bunch of them have fixed within this process.  As they fix, the amount of noise, the number of alleles in the population decreases.  I have not yet measured the number of fixed alleles in the calculation, but I suspect that with the small counts, the reason NS grabs the beneficial mutation so solidly at some point is because the noise has significantly decreased.

Again, of course.

Try this. Assume there are no mutations. Run your simulation starting with your randomized genomes. Your population should evolve rapidly and fitness should fix at a high level. Then when you introduce your beneficial mutation, it will then tend to dominate because it will be distinguishing. Neils only has to outrun Albert.

Quote (bFast @ Mar. 09 2008,18:06)
Now, in real world organisms, there is (almost) always an abundance of available alleles.

Quite the contrary, most organisms, including humans, share almost identical genomes. It's just that we happen to be most interested in the differences. Indeed, this is an important aspect of sexual selection. A seemingly minor difference (a bit better singing voice, an unusual coloration in plumage) can make the crucial difference between a successful mating or not.

Quote (bFast @ Mar. 09 2008,18:06)
This is caused, of course, by other organisms obtaining mutants that have infiltrated the population.

Which is what Allele Blender simulates. New mutations are constantly being introduced. The amount of genetic diversity depends on several factors, including the mutation rate.

Quote (bFast @ Mar. 09 2008,18:06)
My sim suggests that somewhere less than 20,000 is too many, that it produces too much noise for natural selection to filter out, when selecting a beneficial point mutation -- and that, dispite the other sources of noise as described above.

No. Rather, it demonstrates that a near neutral mutation may drift to extinction in a chaotic genomic population. This is what is expected.

Quote (bFast @ Mar. 09 2008,19:00)
In an asexual environment, this would obviously be so.  Which presents a problem.  It would seem that in an asexual environment, the signal to noise issue becomes very much stronger.

Even without recombination, the Allele Blender quickly evolves higher fitness. (And it's much easier to distinguish the lines of descent, being uncrossed lines.) Without mutation also, the population will settle on a high fitness. With mutation, individual mutations, even if beneficial, may be lost, but other mutations will be found.

Try your simulation again, without any mutation first. Take a look at how the  system evolves. Then add some fixed rate of mutation. You'll find that the population more closely resembles biological organisms, complete with families of varieties.

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bFast



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(Permalink) Posted: Mar. 09 2008,22:42   

Zachriel:
Quote
That's a rather odd selection method. You pit organism 1 against organism 2, but it's not the victor that reproduces, but a recombination of two other organisms. I suppose it should result in evolution towards higher fitness, though. I'll test it to be sure.

This is certainly not sexual selection.  But why should we assume that the victor should also get the privelage of reproduction.  Am I to assume that shortly after my handicapped friend I get chased by the bear, and he gets eaten, I get to reproduce?

You will note that when the allele count is 200, this sim works as expected, when it is 2000, it works as expected -- more slowly than the first, but it still evolves.   When the allele count gets to 20,000, genetic drift becomes the predominant paradyme.  This is what I would expect (exactly where the numbers lie is outside of my capacity to predict, but I expected that at some point genetic drift vastly dominates over selection.)  So, as expected, if there are too many alleles in a population, they act as noise, and the signal of the new mutation is drowned out by the noise of all the other alleles flying around everywhere.

Now, the real question is how many alleles are in the average human population?  So far the answer you provided is, "most organisms, including humans, share almost identical genomes."  When the possibility exists of there being 100,000 alleles in the coding DNA of myslef and my wife, in addition there's the active, but not coding DNA (introns, etc.)  When that kind of numbers are being talked about, if 90% of our genes are identical, and the other 10% have an average of 5 alleles, that's still a lot of alleles.  Therefore, within the scope of the numbers that we are dealing with "almost identical" is a pretty mushy term.

Is there a hard estimate of how many alleles are in the population of a typical human community?  (I assume that the alleles in my town are more important to me than additional alleles floating around darkest Africa somewhere.)

  
JAM



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(Permalink) Posted: Mar. 09 2008,23:36   

Quote (bFast @ Mar. 09 2008,22:42)
Now, the real question is how many alleles are in the average human population?

Not at all. The real question is, how many SELECTABLE alleles are there versus how many alleles that produce no change in fitness?
 
Quote
So far the answer you provided is, "most organisms, including humans, share almost identical genomes."  When the possibility exists of there being 100,000 alleles in the coding DNA of myslef and my wife,...

My training is in mammalian genetics, and I have never heard the term "alleles" used in that context. I think you're missing the point.
Quote
...in addition there's the active, but not coding DNA (introns, etc.)  When that kind of numbers are being talked about, if 90% of our genes are identical, and the other 10% have an average of 5 alleles, that's still a lot of alleles.

But not all of them affect fitness.

Moreover, there are genes for which selection drives polymorphism, such as those in the Major Histocompatibility Complex.
 
Quote
Is there a hard estimate of how many alleles are in the population of a typical human community?  (I assume that the alleles in my town are more important to me than additional alleles floating around darkest Africa somewhere.)

That's funny that you should put it in such disturbingly quasi-racist terms, as Africans, being from the cradle of mankind, tend to be much more polymorphic (they have lots more alleles/gene) than any of the human groups that left Africa.

  
bFast



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(Permalink) Posted: Mar. 09 2008,23:59   

JAM, "That's funny that you should put it in such disturbingly quasi-racist terms"

I didn't mean slight.  I only was reaching for a population that was physically the farthest away from me.  I am likely to mate within my community, not a distant community.  The calculations need only reference the assessible genepool, not the total conceivable genepool.

I am still not finding an answer to my question, however.  How many alleles are likely to exist within the human population in the average community.  I can accept that many alleles are "not selectable", "fully neutral".  Fine enough, how many "selectable" alleles are there in a typical community of humans?  

I've been trying to find the answer to the question.  So far I've found the following site: http://books.google.ca/books?i....U&hl=en

It says the following:  
Quote
Perhaps as many as half of the loci in the human population are polymorphic


Quote
the chances of two people who are both "Caucasoid" differing in genetic constitution at one site on a given chromosome are about 14.3 per cent.


If I read this correctly, there's LOTS of alleles!!

  
Bob O'H



Posts: 2132
Joined: Oct. 2005

(Permalink) Posted: Mar. 10 2008,01:21   

bFast - just a couple of observations.
1. It would help if you could clarify your terminology.  I think when you write "alleles" you mean "genes".  In Zachriel's notation, when he has a string of numbers (1112111), each number is a "gene", and each value that a gene can take is an allele.  I think you're describing the same thing, but you're using "allele" when you mean "gene".

Yeah, I know.  Terminology is a pain.  But it will help everyone understand what you're doing.

2. I agree with Zachriel that you have an odd selection scheme.  A "better" scheme might be to select an individual at random to die, and then select the replacement with a probability proportional to the individual's fitness (i.e. divide by the sum of the fitnesses).  Or have a discrete time model and at each generation pick N individuals with replacement with probabilities proportional to the individuals' fitnesses.

3. The reason the focal gene's frequency drifts when there are more genes is that it has a smaller effect on fitness.  If we just think of the binary case, the genetic variance for one gene is p_i(1-p_i) where p_i is the frequency of the 1 allele, and the total genetic variance is sum p_j(1-p_j).  The proportion of variance for one gene is then

p_i(1-p_i)/(sum p_j(1-p_j))

and obviously the sum increases as each new gene is added, so the proportional effect of the ith allele get smaller.  Hence, the effect on fitness is less (because it is the absolute numbers you are using for that), so drift becomes more important.

--------------
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JAM



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Joined: July 2007

(Permalink) Posted: Mar. 10 2008,02:09   

Quote (bFast @ Mar. 09 2008,23:59)
JAM, "That's funny that you should put it in such disturbingly quasi-racist terms"

I didn't mean slight.

It sure seemed that way. You're ignoring my point, which is highly relevant to your question.
Quote
I only was reaching for a population that was physically the farthest away from me.  I am likely to mate within my community, not a distant community.

Does your wife know about this? Seriously, do you not have any African-Americans in your community?
Quote
The calculations need only reference the assessible genepool, not the total conceivable genepool.

Why? You're not making any sense.
Quote
I am still not finding an answer to my question, however.

That's because, as Bob and I have noted, you are mangling the relevant terminology. Hint: geneticists don't use the term "genepool."
Quote
How many alleles are likely to exist within the human population in the average community.

In Africa, or in North Dakota? I can't see how there wouldn't be "average communities" in both places. Or are you hinting at racism again?
Quote
I can accept that many alleles are "not selectable", "fully neutral".

Those are generally described as polymorphisms. There are tens or hundreds of thousands.
Quote
Fine enough, how many "selectable" alleles are there in a typical community of humans?

I don't know, but I know that each of us is heterozygous for 5-10 recessive lethal alleles. Does that help?

The other place to look is in the huge study of Icelandic folks, which would only provide a lower bound, as they are very inbred.
Quote
If I read this correctly, there's LOTS of alleles!!

Is that a problem?

Google's not going to help if you use the wrong terminology.

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 10 2008,09:53   

Quote (bFast @ Mar. 09 2008,22:42)
Zachriel:      
Quote
That's a rather odd selection method. You pit organism 1 against organism 2, but it's not the victor that reproduces, but a recombination of two other organisms. I suppose it should result in evolution towards higher fitness, though. I'll test it to be sure.

This is certainly not sexual selection.  But why should we assume that the victor should also get the privelage of reproduction.  Am I to assume that shortly after my handicapped friend I get chased by the bear, and he gets eaten, I get to reproduce?

Thanks for providing your algorithm. I have reproduced your results. As I had expected, your selection method does result in strong positive selection. Starting from randomized genomes of 0's and 1's, the population rapidly evolves to maximum fitness. With recombination turned on, that's all 1's; 1111111111111111....


   ' This one dies
   If pFit < rFit Then
       r = r1: c = c1
   Else
       r = r2: c = c2
   End If


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bFast



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(Permalink) Posted: Mar. 10 2008,09:53   

JAM, you bore me.  You don't at all answer my real question, but spend all your energy trying to twist what I am saying into something racist.

  
bFast



Posts: 44
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(Permalink) Posted: Mar. 10 2008,09:59   

Zachriel, "Starting from randomized genomes of 0's and 1's, the population rapidly evolves to maximum fitness."

Yes. My algorithm works.  However, the greater the number of alleles, the more slowly any one evolves to maximum fitness.  By about 20,000 they all mostly just wander about aimlessly.

How many alleles that actually do something exist in the average human community?  What is the reasonable number that I should be using when running my sim?

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 10 2008,11:39   

Quote (bFast @ Mar. 09 2008,22:42)
You will note that when the allele count is 200, this sim works as expected, when it is 2000, it works as expected -- more slowly than the first, but it still evolves.   When the allele count gets to 20,000, genetic drift becomes the predominant paradyme.  This is what I would expect (exactly where the numbers lie is outside of my capacity to predict, but I expected that at some point genetic drift vastly dominates over selection.)  So, as expected, if there are too many alleles in a population, they act as noise, and the signal of the new mutation is drowned out by the noise of all the other alleles flying around everywhere.

Of course. So? With a (nearly) neutral mutation, we expect that most will be lost. (With your randomized genome with a size of 2000, the average fitness of each organism is 1000 with a standard deviation of ~22, so a single allele change from a 1 to a 2 is insignificant.) Keep in mind the chance of fixation of a (nearly neutral) mutation is (nearly) equal to the proportion in the population. If at a given locus, 1% of the population has the 2-allele, then we would expect the chance of fixation to be about 1% (perhaps a bit better because there is weak selection).

However, if we introduce the occasional random mutation, the results are strikingly different. The population rapidly evolves by sorting through the randomized 0's and 1's of the genome. Once some order is imposed, the 2-allele then becomes a significant benefit and the selection becomes stronger.

As to your question about natural genetic variations, not only do mutations add variation, but we also have variation due to geographic separation. Your simulation assumes random mating across the population, which will tend to lead to a monomorphic population. However, the Allele Blender uses proximity for both environmental and mating selection. This results in geographic patterns of diversity.

It may be a few days, but I'll try to provide more specifics.

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bFast



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(Permalink) Posted: Mar. 10 2008,12:34   

It seems to me that there are three classes of alleles that are of interest:

- Primarily beneficial alleles, those that have not yet fixed, but eventually will.  Probably a small number.

- Alleles that cause differences between individuals, but are not easily rated as better or worse compared to their sibling alleles.  Like, who's to say that curly hair is better or worse than straight.  In some circomstances one will be favored over another, but hardly with universality.

- Alleles that are functionally identical to their sibs even though they are technically different.  Such as an alternate amino within the same family, causing the same net result.  I think these can be ignored.

So the two numbers of interest are: beneficial alleles, on the rise, and alleles that cause phenotypal differences, but not universal advantage.

As human populations have, until the last couple of centries, been predominantly located into communities, I would assume that numbers from the Icelandic study mentioned by JAM would make sense.

  
bFast



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(Permalink) Posted: Mar. 10 2008,13:14   

Let me just also say, in case it makes for easier numbers, that we don't by any means need human numbers.  We could take numbers from any other species of mammal as far as I am conserned.

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 10 2008,13:22   

Quote (bFast @ Mar. 10 2008,09:59)
Zachriel, "Starting from randomized genomes of 0's and 1's, the population rapidly evolves to maximum fitness."

Yes. My algorithm works.  However, the greater the number of alleles, the more slowly any one evolves to maximum fitness. By about 20,000 they all mostly just wander about aimlessly.

That is not what my results show. With a randomized genome of 20,000 genes (0's and 1's), population of 100, no mutation, your selection algorithm, per generation,

        G        Avr. Fit
        0         10010
        1         10038
        2         10077
        3         10121
        4         10180
        5         10220
        10       10411
        20       10741
        30       10994
        40       11216
        50       11383


In other words, definitely not drift. It's easy to understand why you saw what you wanted to see within these long strings of numbers.

Which brings us to a broader point. Try to hold your own views skeptically. Instead of trying to merely confirm them, try to falsify them. Even if you think you have demonstrated your point, someone might vary the selection algorithm slightly and produce a different result. You have to be able to explain not only your own results, but everyone else's too.


        11326 11428 11409 11396 11408 11411 11333 11380 11334 11369
        11325 11318 11455 11374 11370 11359 11361 11406 11338 11371
        11373 11306 11412 11413 11382 11407 11414 11379 11373 11371
        11407 11370 11387 11398 11326 11365 11417 11397 11405 11420
        11376 11393 11421 11378 11389 11401 11371 11394 11437 11387
        11383 11377 11381 11356 11379 11386 11381 11397 11372 11395
        11339 11400 11383 11353 11351 11425 11411 11384 11408 11386
        11404 11377 11388 11420 11375 11394 11345 11371 11397 11398
        11426 11416 11368 11373 11414 11355 11385 11341 11377 11362
        11383 11358 11408 11363 11355 11396 11345 11448 11362 11372


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J-Dog



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(Permalink) Posted: Mar. 10 2008,13:27   

Quote (bFast @ Mar. 10 2008,13:14)
Let me just also say, in case it makes for easier numbers, that we don't by any means need human numbers.  We could take numbers from any other species of mammal as far as I am conserned.

Welcome to open posting, bfast.  I once was Glarson and DRat so that I could post at UD.

And in honor of your attempt to break free of your brush with the Dark Side, I propose, as you suggested, a non-human mammal species to use with your sim.  

I suggest a mammal covered with blubber, not a lot of brain power, and constantly attempting to increase its breeding opportunities through loud, agressive, and to us here, non-sensical chest beating behaviour.  Of course I am talking about a Walrus (aka DaveScot) and an Innuit woman.

Please put this in your sim for me.  (Although I suspect this will not prove a very fruitful use of your time.)

Thanks,

J-Dog
Banned Twice - And loving it.

--------------
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JAM



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(Permalink) Posted: Mar. 10 2008,15:25   

Quote (bFast @ Mar. 10 2008,09:53)
JAM, you bore me.  You don't at all answer my real question,


Really? How did you conclude that the three responses were not sincere efforts to answer your question at all?

1) There are tens or hundreds of thousands.

2) I don't know, but I know that each of us is heterozygous for 5-10 recessive lethal alleles. Does that help?

3) The other place to look is in the huge study of Icelandic folks, which would only provide a lower bound, as they are very inbred.
Quote
...but spend all your energy trying to twist what I am saying into something racist.

Then why not simply explain what you mean by "average community"? In the context of your question, I have no idea what you mean by that qualification.

I don't think that any twisting is involved in concluding that your trying to exclude "darkest Africa" from your analysis *seems* racist.

  
JAM



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Joined: July 2007

(Permalink) Posted: Mar. 10 2008,15:28   

Quote (bFast @ Mar. 10 2008,12:34)
As human populations have, until the last couple of centries, been predominantly located into communities, I would assume that numbers from the Icelandic study mentioned by JAM would make sense.

So have you changed your mind since you wrote, "You don't at all answer my real question,..."?

I still don't know what you mean by "communities," as average African communities would still be much more polymorphic than average European or Asian communities.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 10 2008,15:29   

J-Dog:
Quote
Of course I am talking about a Walrus (aka DaveScot) and an Innuit woman.


I was actually quite seriously thinking that we may know more about alleles that do stuff in dogs, as dogs have been bread from wolves into so many varieties.  So maybe we have a better logging of the effect of various alleles in dogs/wolves than in other mammals, such as walruses.  Oh yea, we'll have to include your genes.

  
bFast



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Joined: Mar. 2008

(Permalink) Posted: Mar. 10 2008,15:32   

JAM, the numbers available for the Icelandics seems just ducky as I suggested two posts back.  Though we may see the Icelandic community as "ingrown" by modern standards, I suspect that 200 years ago, (most of human evolution happened before 200 years ago, yes?) or 500 years ago, small, relatively isolated communities were much more common than they did now.  Selecting for an isolated community should produce a smaller allele count than would a count of all alleles within humanity.

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 10 2008,20:25   

Quote (bFast @ Mar. 09 2008,22:42)
(I assume that the alleles in my town are more important to me than additional alleles floating around darkest Africa somewhere.)

Quote (bFast @ Mar. 10 2008,12:34)
As human populations have, until the last couple of centries, been predominantly located into communities, I would assume that numbers from the Icelandic study mentioned by JAM would make sense.

There is more variation within human populations (~85%) than between human populations (~15%).



Any two random humans has about 99.99% sequence similarity. Most of these differences are biologically insignificant, a point that JAM alluded to above.

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bFast



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(Permalink) Posted: Mar. 10 2008,22:09   

1, You seem to be saying that local community or scope of humanity makes little difference.  Fine enough.

2, You suggest that you and I are 99.99% identical.  If there are 25,000 genes, with an average of 100 aminos per gene, that would mean that there's about 250 alleles.  From my understanding there are at least seven alleles that control for eye color (I recognize that these alleles may have other effects, as is so common.)  So eye color eats up 35% of the available alleles.  I don't believe it for a moment.  My bet is that there is no less than 1000 alleles that affect the phenotype within humanity.  Even 1000 would be an amazingly small number considering the amount of variance within humanity.  Further, if there really are this few alleles, getting to an accurate cause for all genetically caused diseases should be pretty darn easy.

"There are over 6000 genetic disorders that can be passed down through generations." (http://www.geneticdiseasefoundation.org/) That would indicate that there are 6 genetic disorders for every allele. ;)

  
bFast



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(Permalink) Posted: Mar. 10 2008,22:27   

Oops, math error.  7 in 250 is about 2.8% of the alleles that control eye color.

  
Henry J



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Joined: Mar. 2005

(Permalink) Posted: Mar. 10 2008,23:13   

Quote
If there are 25,000 genes, with an average of 100 aminos per gene, that would mean that there's about 250 alleles.


Wouldn't that 250 be only the ones that happen to differ between the two individuals being compared? Other individuals could have different alleles for those 250 genes or for other genes that were the same in the two that were being compared here.

Henry

  
Wesley R. Elsberry



Posts: 4807
Joined: May 2002

(Permalink) Posted: Mar. 10 2008,23:19   

Quote (bFast @ Mar. 10 2008,22:09)
1, You seem to be saying that local community or scope of humanity makes little difference.  Fine enough.

2, You suggest that you and I are 99.99% identical.  If there are 25,000 genes, with an average of 100 aminos per gene, that would mean that there's about 250 alleles.  From my understanding there are at least seven alleles that control for eye color (I recognize that these alleles may have other effects, as is so common.)  So eye color eats up 35% of the available alleles.  I don't believe it for a moment.  My bet is that there is no less than 1000 alleles that affect the phenotype within humanity.  Even 1000 would be an amazingly small number considering the amount of variance within humanity.  Further, if there really are this few alleles, getting to an accurate cause for all genetically caused diseases should be pretty darn easy.

"There are over 6000 genetic disorders that can be passed down through generations." (http://www.geneticdiseasefoundation.org/) That would indicate that there are 6 genetic disorders for every allele. ;)


Amino acids are specified by 3 nucleotide bases.

25,000 * 100 * 3 / 10,000 = 750

Edit: I missed another obvious factor: two copies per individual, thus:

25,000 * 100 * 3 * 2 / 10,000 = 1,500

That would be the estimate given the numbers you give for the expected number of nucleotide bases different between any two members of the population in question, and not an estimate of the total number of alternative alleles in the population. That number would be far, far larger for any reasonable-sized population.

I also think the average AA length of proteins is skimpy in your estimate, but that's a really minor error, comparatively.

 
Quote

From my understanding there are at least seven alleles that control for eye color (I recognize that these alleles may have other effects, as is so common.)


Here's a useful piece of trivia: Between any two organisms whose genetics are based on paired chromosomes, the total number of alleles that they can possibly represent at any one locus is four.

Edited by Wesley R. Elsberry on Mar. 11 2008,00:08

--------------
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Richard Simons



Posts: 425
Joined: Oct. 2006

(Permalink) Posted: Mar. 11 2008,05:31   

bfast, I am not convinced that you have the concept of alleles completely straight as you use the word in an idiosyncratic manner.
Quote
My bet is that there is no less than 1000 alleles that affect the phenotype within humanity.

Here you seem to be using allele when you actually mean locus. If we think of genes as being strung out along a chromosome, each position is referred to as a locus. At some of the loci there may be variants in the gene, called alleles. In a diploid organism, such as humans, each individual can, at most, have just two alleles for any one trait even though in the population as a whole there may be hundreds of alleles for this trait.

It is not normal to refer to people as differing by a certain number of alleles, partly because what do you if two people are heterozygous and have three alleles between them? I suspect part of the problem may be that the word 'gene' is used in two ways. It usually means 'locus' but is also used to mean 'allele' so whenever you see it you need to be sure which meaning is intended.

I am writing this in the middle of the night because I could not sleep. I hope I don't look at it in the morning and realize it is really obtuse.

--------------
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Zachriel



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(Permalink) Posted: Mar. 11 2008,07:03   

bFast, this was an interesting project. I just don't think it shows what you think it does. Nor have you cast the skeptical eye towards your preconceived notions, as I suggested you do.

Quote (bFast @ Mar. 10 2008,22:09)
1, You seem to be saying that local community or scope of humanity makes little difference.  Fine enough.

They are certainly not negligible, not to humans anyway. Some non-humans might have trouble telling the difference. Unlike Allele Blender, your simulation does not account for proximity. This tends to mix and homogenize the population.

Quote (bFast @ Mar. 10 2008,22:09)
If there are 25,000 genes, with an average of 100 aminos per gene, that would mean that there's about 250 alleles.

Between two individuals, not throughout the population. Gene size is usually in the few kilobyte range. Of course, we are only concerned with environmentally selectable differences, so there may be innumerable flavors all represented by 1's. In any case, unlike Allele Blender, your simulation only allows for three selectable alleles per locus throughout the population.

Quote (bFast @ Mar. 10 2008,22:09)
From my understanding there are at least seven alleles that control for eye color (I recognize that these alleles may have other effects, as is so common.)  So eye color eats up 35% of the available alleles. I don't believe it for a moment.

Many alleles may be neutral. Other alleles may be partially or wholly due to mating selection. Again, unlike Allele Blender, your simulation does not account for mating selection (for fitness or arbitrary trait).

There are also other polymorphisms, such as duplications, insertions, deletions, rearrangements, and linked traits that are not considered in either simulation.

This doesn't mean the simulations are without value. But even within the limited venue of your own simulation, you have yet to justify your preconceived conclusions.

SOME OUTSTANDING QUESTIONS:

* You claim that some beneficial mutations can be lost in genomes that vary wildly in fitness. So!? This is the expected result.

* You claimed, incorrectly, that your random genomes of sufficiently large size would not evolve directionally. This was incorrect.

* Mating selection in Allele Blender for a non-beneficial trait still allows for rapid improvement in fitness.

* If we introduce the occasional random mutation, the results are strikingly different. The population rapidly evolves by sorting through the randomized 0's and 1's of the genome. Once some order is imposed, the 2-allele then becomes a significant benefit and the selection becomes stronger.

* The real question is, how many SELECTABLE alleles are there versus how many alleles that produce no change in fitness? — JAM

* As to your question about natural genetic variations, not only do mutations add variation, but we also have variation due to geographic separation. Your simulation assumes random mating across the population, which will tend to lead to a monotypic population. However, the Allele Blender uses proximity for both environmental and mating selection. This results in geographic patterns of diversity.

I'll try to clean up the code on Allele Blender in a few days, so you can experiment with it.


   ' Child's Fitness
   cFit = calcFitness(Child)
   ' Find weakest in area, including Parent
   minFit = pFit
   For f = 1 To 9
       fit(f) = Fitness(r + ro(f), c + co(f))
       If fit(f) > 0 And fit(f) < minFit Then minFit = fit(f)
   Next f


   ' If Child is better than anyone in the Neighborhood,
   '   then replace the weakest

   If cFit > minFit Then

       ' Count weaklings in Neighborhood
       w = 0
       For f = 1 To 9
           If fit(f) = minFit Then
               w = w + 1
               weak(w) = f
           End If
       Next f


       ' Replace the weakest in Neighborhood
       If w > 0 Then
           weakest = Random(1, w)
           rx = r + ro(weak(weakest))
           cx = c + co(weak(weakest))


           ' Update Array
           Population(rx, cx) = Child
           Fitness(rx, cx) = cFit
           Beautiful(rx, cx) = calcBeauty(Child)


           ' Update Display
           Worksheets("Fitness").Cells(rx, cx) = Fitness(rx, cx)
           Worksheets("Sequence").Cells(rx, cx) = Population(rx, cx)
           Worksheets("Beauty").Cells(rx, cx) = Beautiful(rx, cx)
       Else
           Stop
   ' Just checking
       End If
   End If


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Zachriel



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(Permalink) Posted: Mar. 11 2008,07:38   

Quote (Zachriel @ Mar. 11 2008,07:03)
* You claim that some beneficial mutations can be lost in genomes that vary wildly in fitness. So!? This is the expected result.

Perhaps some examples would help.

* A hunting dog with a refined sense of smell but who would rather sleep than hunt.
* A graceful gazelle without a sense of danger.
* A smart kid with a reckless streak regarding cars.

(Each of these traits might be beneficial in certain environments.)

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slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 11 2008,08:29   

[quote=bFast,Mar. 10 2008,22:09][/quote]
Wow...
bfast:
Quote

2, You suggest that you and I are 99.99% identical.  If there are 25,000 genes, with an average of 100 aminos per gene, that would mean that there's about 250 alleles.

What does the average amino acid number have to do with it?  How you get 250 alleles out of that is a mystery of creationist math and biology.
Quote

From my understanding there are at least seven alleles that control for eye color (I recognize that these alleles may have other effects, as is so common.)  So eye color eats up 35% of the available alleles.  I don't believe it for a moment.

What you 'believe' or not is immaterial.
Quote

My bet is that there is [sic] no less than 1000 alleles that affect the phenotype within humanity.  Even 1000 would be an amazingly small number considering the amount of variance within humanity.


Why is that?  Do you have a rationale for that statement?  How much change does an allele produce?  Is it quantifiable?  Do all alleles produce the same or similar amount of change?  And how do you know?
Quote

 Further, if there really are this few alleles, getting to an accurate cause for all genetically caused diseases should be pretty darn easy.

"There are over 6000 genetic disorders that can be passed down through generations." (http://www.geneticdiseasefoundation.org/) That would indicate that there are 6 genetic disorders for every allele. ;)
You demonstrate nicely a common problem with IDcreationists with no biology background attempting to pontificate on biological matters.   For starters, why do you assume a completely uniform distribution of allelic difference?

  
bFast



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(Permalink) Posted: Mar. 11 2008,11:30   

Richard Simons:
Quote
bfast, I am not convinced that you have the concept of alleles completely straight as you use the word in an idiosyncratic manner.
Quote

My bet is that there is no less than 1000 alleles that affect the phenotype within humanity.


Here you seem to be using allele when you actually mean locus.


No, I actually mean allele.  An allele is a variant of the same protein.  Somewhere in the genome there is a protein that controls for eye color.  One variant produces blue eyes, the other produces brown eyes.  Likely the allele producing green eyes is a third allele of the same protein.  Honest, I doubt if I could have carried this conversation on this long with Zachriel if I was unaware of what an allele is.

  
bFast



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(Permalink) Posted: Mar. 11 2008,11:35   

Zachriel, this conversation really needs a hard (or reasonably hard) number of how many alleles affect the phenotype of the human population.  I would suggest that any allele that produces a noticeable effect of any sort should be counted.  Though eye color may not affect one's ability to fight a bear, it may may a big difference with any one mating opportunity.

Zachriel: [QUOTE]bFast, this was an interesting project/QUOTE]
I am working on a more advanced sim that integrates two of the other sources of noise that I suggested in the beginning.

Quote
I just don't think it shows what you think it does. Nor have you cast the skeptical eye towards your preconceived notions, as I suggested you do.

This sword cuts both ways.  I don't see you risking your preconceived notions on this sim any more than I am.

  
oldmanintheskydidntdoit



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(Permalink) Posted: Mar. 11 2008,11:40   

Quote (bFast @ Mar. 11 2008,11:35)
I don't see you risking your preconceived notions on this sim any more than I am.

For the benefit of the reader who is not familiar with the background here, why not list these "preconceived notions" to ensure no misunderstandings arise? If they are contributing to the design of the sim anyway....

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JAM



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(Permalink) Posted: Mar. 11 2008,12:25   

Quote (bFast @ Mar. 11 2008,11:30)
Richard Simons:      
Quote
bfast, I am not convinced that you have the concept of alleles completely straight as you use the word in an idiosyncratic manner.
   
Quote

My bet is that there is no less than 1000 alleles that affect the phenotype within humanity.


Here you seem to be using allele when you actually mean locus.


No, I actually mean allele.

No, you don't.
 
Quote
An allele is a variant of the same protein.

Wrong. Alleles are variants of genes. We've since expanded the definition to refer to polymorphisms outside of genes, like SNPs.

Only a minority of alleles cause the production of different proteins. Only a minority of those alleles change the function of proteins.
 
Quote
Somewhere in the genome there is a protein that controls for eye color.

Your terminology is completely wrong, and it prevents you from understanding and communicating the most basic concepts.

There are no proteins in the genome.

There are genes throughout the genome that encode proteins involved in eye color.

To say that this "controls" eye color is, strictly speaking, incorrect. The products of two genes are simply required to produce pigment in the iris. People who are homozygous null at both loci have blue eyes.
 
Quote
One variant produces blue eyes, the other produces brown eyes.

That's an oversimplification.
 
Quote
Likely the allele producing green eyes is a third allele of the same protein.

No, for two reasons. There's no such thing as "an allele of a protein," because alleles are versions of genes (aka loci). The second reason is that there is a second locus, EYCL1, to which green color is largely (but not completely) attributed. Then, there's epistatic interactions.
 
Quote
Honest, I doubt if I could have carried this conversation on this long with Zachriel if I was unaware of what an allele is.

That's why we're laughing at you.

  
slpage



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(Permalink) Posted: Mar. 11 2008,13:09   

[quote=bFast,Mar. 11 2008,11:30][/quote]
Clueless creationist....


Quote
Richard Simons:  
Quote
bfast, I am not convinced that you have the concept of alleles completely straight as you use the word in an idiosyncratic manner.
 
Quote

My bet is that there is no less than 1000 alleles that affect the phenotype within humanity.


Here you seem to be using allele when you actually mean locus.


No, I actually mean allele.  An allele is a variant of the same protein.  


Do you even know what a GENE is for christ's sake?

No, an allele is a variant form of a GENE.

You should stick to whatever it is you think you actually understand, because this ain't it.
Quote




Somewhere in the genome there is a protein that controls for eye color.


Clueless.  I may be distracting from is topic, but you should not even be discussing it with this level of ignorance.
Quote

 Honest, I doubt if I could have carried this conversation on this long with Zachriel if I was unaware of what an allele is.


Well, you have been yet you are very clearly unaware.

Creationists have never let their ignorance stop them from pontificating, though.  So keep going - it is entertaining to see someone so clueless carry on as if they have some sort of in-depth understanding.

  
Wesley R. Elsberry



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(Permalink) Posted: Mar. 11 2008,13:11   

Here's the t.o. jargon file entry:

Quote

:Allele:
   (n) [FAQ] 1. One of two or more forms [of a {gene}] that can exist at a single locus. [den., from Suzuki et al. 1989] "If one of your parents has blue eyes and yours are brown, then you have two different alleles of the eye color gene -- one for blue and one for brown."


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Wesley R. Elsberry



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(Permalink) Posted: Mar. 11 2008,14:12   

Researchers aren't confused about what an allele is...

 
Quote

The presence of a multitude of protein isoforms, such as splice variants, combinatorial variants, post-translational modifications, specific proteolysis, and genetic variability (alleles), makes the human proteome space huge, and the initial ambition of a genome-wide antibody-based proteomics effort has therefore been suggested to be directed to the non-redundant proteome defined as a representative protein from every gene locus (3). The current estimate of the size of the non-redundant proteome is ~23,000 proteins (Ensembl, www.ensembl.org), and at present more than 16,000 of those have been manually annotated by the Swiss-Prot/UniProt effort (www.uniprot.org).


Emphasis added.

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bFast



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(Permalink) Posted: Mar. 11 2008,14:19   

Wesley Elsberry, thanks for getting to a real number to my question.

Based upon this information, it it reasonable to use the number 16,000 as the number of alleles in the human population?

  
Wesley R. Elsberry



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(Permalink) Posted: Mar. 11 2008,14:21   

If bFast hasn't read it yet, it is time to dig into Chris Colby's "Introduction to Evolutionary Biology", one of the "must-read" FAQs on the TalkOrigins Archive.

Quote

Evolution requires genetic variation. If there were no dark moths, the population could not have evolved from mostly light to mostly dark. In order for continuing evolution there must be mechanisms to increase or create genetic variation and mechanisms to decrease it. Mutation is a change in a gene. These changes are the source of new genetic variation. Natural selection operates on this variation.

Genetic variation has two components: allelic diversity and non- random associations of alleles. Alleles are different versions of the same gene. For example, humans can have A, B or O alleles that determine one aspect of their blood type. Most animals, including humans, are diploid -- they contain two alleles for every gene at every locus, one inherited from their mother and one inherited from their father. Locus is the location of a gene on a chromosome. Humans can be AA, AB, AO, BB, BO or OO at the blood group locus. If the two alleles at a locus are the same type (for instance two A alleles) the individual would be called homozygous. An individual with two different alleles at a locus (for example, an AB individual) is called heterozygous. At any locus there can be many different alleles in a population, more alleles than any single organism can possess. For example, no single human can have an A, B and an O allele.

Considerable variation is present in natural populations. At 45 percent of loci in plants there is more than one allele in the gene pool. [allele: alternate version of a gene (created by mutation)] Any given plant is likely to be heterozygous at about 15 percent of its loci. Levels of genetic variation in animals range from roughly 15% of loci having more than one allele (polymorphic) in birds, to over 50% of loci being polymorphic in insects. Mammals and reptiles are polymorphic at about 20% of their loci - - amphibians and fish are polymorphic at around 30% of their loci. In most populations, there are enough loci and enough different alleles that every individual, identical twins excepted, has a unique combination of alleles.


That essay has been there since the mid-1990s.

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Wesley R. Elsberry



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(Permalink) Posted: Mar. 11 2008,14:25   

Quote (bFast @ Mar. 11 2008,14:19)
Wesley Elsberry, thanks for getting to a real number to my question.

Based upon this information, it it reasonable to use the number 16,000 as the number of alleles in the human population?

No. The very paragraph quoted notes that their research is ignoring the various sources of variation listed, including allelic variation. They just want to accumulate one representative protein per genetic locus, and thus will take the result of protein assembly from only one allele per locus. Nor is 16,000 even the number to use for that limited prospect, since that just happens to be how many proteins have been manually annotated so far in one project.

ETA: For the eye color example, the project quoted would likely register only two proteins for the two major loci known for eye color, though we happen to know that there are more protein products associated with those loci.

Edited by Wesley R. Elsberry on Mar. 11 2008,14:29

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Zachriel



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(Permalink) Posted: Mar. 11 2008,14:29   

Quote (bFast @ Mar. 11 2008,11:35)
Zachriel, this conversation really needs a hard (or reasonably hard) number of how many alleles affect the phenotype of the human population.  I would suggest that any allele that produces a noticeable effect of any sort should be counted.  Though eye color may not affect one's ability to fight a bear, it may may a big difference with any one mating opportunity.

You are getting a bit ahead of yourself. Biology is far more complicated than these sorts of simulations which are only tangentially related to living organisms. You haven't even been able to sustain your simple point concerning noise within the toy universe.

Quote (bFast @ Mar. 11 2008,11:35)
Zachriel:    
Quote
I just don't think it shows what you think it does. Nor have you cast the skeptical eye towards your preconceived notions, as I suggested you do.

This sword cuts both ways.  I don't see you risking your preconceived notions on this sim any more than I am.

Huh? I even replicated your own algorithm so that I could study its behavior in detail. Moreover, for some reason, you seem to have forgotten to address these points:

* You claimed that some beneficial mutations can be lost in genomes that vary wildly in fitness. So!? This is the expected result.

* You claimed, incorrectly, that your random genomes of sufficiently large size (20K) would not evolve directionally. This was incorrect.

* If we introduce the occasional random mutation, the results are strikingly different.

The goal isn't to prove that a particular system works the way you think it should. You need to generalize your results to include a sufficiently large class of evolutionary algorithms that is might reasonably shed light on the behavior of biological systems.

I would suggest you continue to study your simple system to better understand how it works and why you were wrong about its behavior. It's sufficient to its purpose.

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bFast



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(Permalink) Posted: Mar. 11 2008,14:50   

I have added a few features to my sim.  Most noteably I have added an excel compatible summary output.  The computer is now producing a mass simulation.  When we get real data to work with, we can examine the results with a higher data to presumption ratio.

  
Wesley R. Elsberry



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(Permalink) Posted: Mar. 11 2008,15:04   

One could get a back-of-the-envelope guess for a minimum number of alleles in the human population by combining Colby's information with that of the quoted proteomic project. I worked that out, but I figure that maybe I can pose it as an exercise for the reader here.

I don't get, though, what a "estimated total number of alleles" is supposed to do for you once you've got it. AFAICT, one cannot use the number in a unitary fashion.

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bFast



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(Permalink) Posted: Mar. 11 2008,15:17   

Wesley R. Elsberry, "one cannot use the number in a unitary fashion."

Why not?

  
Wesley R. Elsberry



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(Permalink) Posted: Mar. 11 2008,15:24   

Quote (bFast @ Mar. 11 2008,15:17)
Wesley R. Elsberry, "one cannot use the number in a unitary fashion."

Why not?

Tell me how you propose using it and I'll tell you whether that makes sense to me.

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JAM



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(Permalink) Posted: Mar. 11 2008,16:31   

Quote (bFast @ Mar. 11 2008,14:19)
Wesley Elsberry, thanks for getting to a real number to my question.

But no thanks to those who corrected your gross misunderstanding of the fundamentals you need to understand to construct a useful model.

Never admit an error, bfast. That does wonders for your credibility.

  
bFast



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(Permalink) Posted: Mar. 11 2008,18:30   

Wesley R. Elsberry, "Tell me how you propose using it and I'll tell you whether that makes sense to me."

Please read my original post, post #19 on page 1.

  
bFast



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(Permalink) Posted: Mar. 11 2008,18:31   

JAM, and the other peanut gallery critics,  has it dawned on you that Zachriel, an actual Ph.D. biologist, has not questioned my understanding of what an allele is.  Convince him that I misunderstand or SHUT UP!!

  
Zachriel



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(Permalink) Posted: Mar. 11 2008,18:53   

Quote (bFast @ Mar. 11 2008,18:31)
JAM, and the other peanut gallery critics,  has it dawned on you that Zachriel, an actual Ph.D. biologist, has not questioned my understanding of what an allele is. Convince him that I misunderstand or SHUT UP!!

I think you're confused. Zachriel is the angel that rules over memory, presides over the planet Jupiter. Crystal spheres, that sort of thing. JAM, on the other hand, says he's trained in mammalian genetics. Of mice and men.

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JAM



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(Permalink) Posted: Mar. 11 2008,18:57   

Quote (bFast @ Mar. 11 2008,18:31)
JAM, and the other peanut gallery critics,  has it dawned on you that Zachriel, an actual Ph.D. biologist, has not questioned my understanding of what an allele is.  Convince him that I misunderstand or SHUT UP!!

bFast,

It's clear to me that Zachriel knows full well that you don't understand what an allele is.

Given your petulant whining, that would be clear to me even if I was a lay observer instead of the Ph.D. biologist that I actually am.

It's hysterically funny that you take the fact that Zachriel didn't correct you as some sort of endorsement of your false claim that alleles are versions of proteins.

bFast, Mar. 10 2008,09:53  
"JAM, you bore me.  You don't at all answer my real question..."

bFast, less than 3 hours later:
"I would assume that numbers from the Icelandic study mentioned by JAM would make sense."

  
Wesley R. Elsberry



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(Permalink) Posted: Mar. 11 2008,19:07   

Quote (bFast @ Mar. 11 2008,18:30)
Wesley R. Elsberry, "Tell me how you propose using it and I'll tell you whether that makes sense to me."

Please read my original post, post #19 on page 1.

Yes. What you want is the proportion of polymorphic loci, not the absolute number of alleles. There are broad numbers in the Colby FAQ.

Alleles are not variants of proteins, they are variants of genes. I am a Ph.D. biologist, by the way.

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Wesley R. Elsberry



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(Permalink) Posted: Mar. 11 2008,20:24   

By the way, Sir Ronald Fisher has analytic solutions for many of the problems proposed in this thread. See "The Genetical Theory of Natural Selection", 1930.

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Richard Simons



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(Permalink) Posted: Mar. 11 2008,21:00   

Quote (bFast @ Mar. 11 2008,11:30)
An allele is a variant of the same protein.  Somewhere in the genome there is a protein that controls for eye color.

No, alleles are not proteins. Although in the 1950s it was thought that the genetic material might be protein it has been known for over 40 years that is nucleic acids.

 
Quote (bFast @ Mar. 11 2008,18:31)
JAM, and the other peanut gallery critics,  has it dawned on you that Zachriel, an actual Ph.D. biologist, has not questioned my understanding of what an allele is.  Convince him that I misunderstand or SHUT UP!!

That Zachriel has not blatently criticized your use of allele does not make it correct. I too have a Ph.D., perhaps not in genetics but I have taken several post-graduate courses in plant breeding. Your usage of 'allele' has been, shall we say, different.

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bFast



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(Permalink) Posted: Mar. 11 2008,21:28   

Wesley R. Elsberry, "Alleles are not variants of proteins, they are variants of genes. I am a Ph.D. biologist, by the way."

I am aware that alleles are variants of genes. But genes make proteins, amongst other stuff that they do.  Often coding genes vary in a way that doesn't affect the resultant protein.  As such, the variant is not selectable, and is ignorable in this context.  Often the resultant change in the protein is the switch of one amino for another which does not affect the protein in any way.  I also respect the hypothesis that about 95% of DNA does absolutely nothing for the organism, therefore any change in that 95% does nothing.

Only alleles of genes (two variants of the same gene) which actually affect the phenotype of the organism need be considered in this context.  I actually understand all of that.

Now, back to the first question.  How many alleles are there which affect the organism's phenotype (in this case a mammal, I don't care which one) in any measurable way?  

JAM:
Quote
bFast, less than 3 hours later:
"I would assume that numbers from the Icelandic study mentioned by JAM would make sense."

You still haven't given me the darn number!!

I understand perfectly what an allele is.  You all are just playing the "creationists aren't evolutionists because they don't understand the basics" card.  It is bull!

If I get any more of it, I will end this thread.  I am getting interesting results on my extended simulation, but I think I'll find a less rejecting audience.

  
bFast



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(Permalink) Posted: Mar. 11 2008,21:31   

Oh, by the way.  I am also aware that genes often code for more than one protein, that genes sometime code for active RNA sequences, and that genes play various "control" roles.  Any of these genes could have multiple versions floating around, each "multiple version" is an allele.  If the versions affect the organism's phenotype in any way, whether it be the organism's fight/flight respons, or the length of its eye-lashes then it should "count" in this context.  If two alleles make no difference to the phenotype they should be ignored.

  
bFast



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(Permalink) Posted: Mar. 11 2008,21:40   

And, gentlemen, if my understanding of alleles is so messed up, why could Zachriel simulate my ideas in his pre-built allele simulating software?  Answer me that one?

  
Zachriel



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(Permalink) Posted: Mar. 11 2008,22:00   

I ran a very interesting trial with bFast's simulator. Population 400, genes 500. At generation 71, all 500 genes were 1's. Doing a little ID math, that's 2^500. The Universal Probability Bound! And not just once! The entire population. (By the way, if the population is too small, there's a significant chance that a particular locus will not have an available 1-allele. His simulation does not allow novel mutations.)

Now with Allele Blender, we can mutate from a 1-allele to a 2-allele with a probability of 20%. From a 2-allele to a 3-allele also with a probability of 20%. And stepping up to the 9-allele. For any particular gene to reach the 9-allele is eight steps or ~10^-6. Population 400, genes 100. At generation 369, we reached saturation. All 9's. Every gene throughout the population. The ID math is 10^-600.





   ' Fitness and Beauty Stats
   cntFitness = 0: minFitness = Fitness(1, 1): maxFitness = minFitness
   cntBeauty = 0: minBeauty = Beautiful(1, 1): maxBeauty = minBeauty

   For r = 1 To numRows
     For c = 1 To numCols

       f = Fitness(r, c)
       cntFitness = cntFitness + f
       If f > maxFitness Then maxFitness = f
       If f < minFitness Then minFitness = f

       b = Beautiful(r, c)
       cntBeauty = cntBeauty + b
       If b > maxBeauty Then maxBeauty = b
       If b < minBeauty Then minBeauty = b

     Next c
   Next r

   avrFitness = cntFitness / (numRows * numCols)
   avrBeauty = cntBeauty / (numRows * numCols)


And it took less than zillions of years

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digitus impudicus



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(Permalink) Posted: Mar. 11 2008,22:01   

At first guess, I would say that he made a decision to use the appropriate definition of an allele in the model.....

We now return you to your lurker free channel

  
slpage



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(Permalink) Posted: Mar. 12 2008,08:08   

Quote (bFast @ Mar. 11 2008,18:31)
JAM, and the other peanut gallery critics,  has it dawned on you that Zachriel, an actual Ph.D. biologist, has not questioned my understanding of what an allele is.  Convince him that I misunderstand or SHUT UP!!

Sorry, bfast, I too have a PhD in biology (anatomy and cell biology, to be precise) and you clearly don't even really understand what a gene is, much less an allele.

Here, I will prove it:

"An allele is a variant of the same protein. "


An allele is not a protein.  Nor is a gene.  You clearly don't know, whether Zachrial pointed it out or not.  Maybe he just has a higher tolerance for arrogant ignorance.


Perhaps YOU should SHUT UP since you are clearly well out of your league on this basic issue.

  
slpage



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(Permalink) Posted: Mar. 12 2008,08:11   

Quote (bFast @ Mar. 11 2008,21:40)
And, gentlemen, if my understanding of alleles is so messed up, why could Zachriel simulate my ideas in his pre-built allele simulating software?  Answer me that one?

Simulators do not rely on erroneous understandings, they use numbers.  Pretty simple, really.


But, you are a computer technician creationist, and you know everything about everything.

  
slpage



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(Permalink) Posted: Mar. 12 2008,08:22   

Quote (bFast @ Mar. 11 2008,21:28)

bfast:
Quote
I am aware that alleles are variants of genes. But genes make proteins, amongst other stuff that they do.

Yes, but they are not proteins.
Google expertise is not real expertise.
Quote
Only alleles of genes (two variants of the same gene) which actually affect the phenotype of the organism need be considered in this context.  I actually understand all of that.

Yet you wrote that alleles are variations of proteins, so clearly you don't.  If it had been a mere misstatement, then you would have had no problem admitting the error and moving on. But you actually expanded on the error:

No, I actually mean allele.  An allele is a variant of the same protein.  Somewhere in the genome there is a protein that controls for eye color.  One variant produces blue eyes, the other produces brown eyes.  Likely the allele producing green eyes is a third allele of the same protein.

And now you are attempting to minimize/equivocate by offering up some Wiki expertise (that still seems to ignore the resources Wes provided).
Quote

Now, back to the first question.  How many alleles are there which affect the organism's phenotype (in this case a mammal, I don't care which one) in any measurable way?  

Who knows?  Maybe you can ask DaveScot - he has a high IQ.
Quote

I understand perfectly what an allele is.  You all are just playing the "creationists aren't evolutionists because they don't understand the basics" card.  It is bull!


An allele is a variant of the same protein.  Somewhere in the genome there is a protein that controls for eye color.  One variant produces blue eyes, the other produces brown eyes.  Likely the allele producing green eyes is a third allele of the same protein.

'Bull' must be creationese for 'true'.
Quote

If I get any more of it, I will end this thread.  I am getting interesting results on my extended simulation, but I think I'll find a less rejecting audience.


You mean like a bunch of sycophantic know-nothing fellow creationists who seem to live to pat each other on the back for spewing nonsense on moderator-protected creationist havens like UD?

What a spoiled baby.

  
Zachriel



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(Permalink) Posted: Mar. 12 2008,09:08   

Quote (slpage @ Mar. 12 2008,08:08)
You clearly don't know, whether Zachrial pointed it out or not.  Maybe he just has a higher tolerance for arrogant ignorance.

I did try to clarify bFast's terminology earlier in the thread in order to fully comprehend what he was trying to claim. However, he hasn't been too forthcoming on answering my questions. I am still willing to give him a chance to make his point.

(The problem remains of how to generalize the results sufficiently as to make a valid claim about biology. I remain very doubtful. The results so far actually contradict bFast's understanding—even within the toy universe. But first things first.)

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slpage



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(Permalink) Posted: Mar. 12 2008,09:22   

Quote (Zachriel @ Mar. 12 2008,09:08)
Quote (slpage @ Mar. 12 2008,08:08)
You clearly don't know, whether Zachrial pointed it out or not.  Maybe he just has a higher tolerance for arrogant ignorance.

I did try to clarify bFast's terminology earlier in the thread in order to fully comprehend what he was trying to claim. However, he hasn't been too forthcoming on answering my questions. I am still willing to give him a chance to make his point.

(The problem remains of how to generalize the results sufficiently as to make a valid claim about biology. I remain very doubtful. The results so far actually contradict bFast's understanding—even within the toy universe. But first things first.)

Indeed.

This reliance upon 'toy' examples has a long history in the IDcreationist realm.  I am reminded of Cordova's insistence that his "toy example" (his words) of molecular phylogenetics - employing a whopping 10 letters, 'mutating' 1 per round of 'evolution', and showing that after only a few such rounds, hierarchies were impossible to make - proved that molecular phylogenetics was unrelaiable and also, of course, that somehow this showed evolution was wrong.  This occurred on the old version of the KCFS forum.  To employ a hackneyed phrase, it wasn't even wrong, and here we have a simulator violating Borel's theorem right before the creationist's eyes.  Amazing.

In the end, my 'predicition' was right - you just have a higher tolerance for arrogant ignorance. :p

  
bFast



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(Permalink) Posted: Mar. 12 2008,10:41   

Zachriel, "I am still willing to give him a chance to make his point."

As I mentioned earler, I have modified my sim to log its results, and to do a run, advance, run cycle.  I am also running a pure-random baseline, so that we can see exactly what genetic drift will do.  When I have a package of serious data, then there will be results to talk about.

Zachriel:
Quote
I did try to clarify bFast's terminology earlier in the thread in order to fully comprehend what he was trying to claim. However, he hasn't been too forthcoming on answering my questions.


Which question have I not been forthcoming about?

I have placed one question before you all that I haven't had an answer to yet.  How many alleles are there in the human, or another mammal's, population that directly affect the phenotype.  What number should I be using for my gene count?  So far I have numbers from the unbelievably low 250, to a high of 16,000.  However, whether the 16,000 all register a difference in the human phenotype is not clear.

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Mar. 12 2008,10:55   

Quote (oldmanintheskydidntdoit @ Mar. 11 2008,11:40)
 
Quote (bFast @ Mar. 11 2008,11:35)
I don't see you risking your preconceived notions on this sim any more than I am.

For the benefit of the reader who is not familiar with the background here, why not list these "preconceived notions" to ensure no misunderstandings arise? If they are contributing to the design of the sim anyway....

Hi bFast,
I asked you what preconceived notions were feeding into the design of your sim. What notion is it that you hope your sim will support, once sufficient data is available?

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
JAM



Posts: 517
Joined: July 2007

(Permalink) Posted: Mar. 12 2008,11:47   

Quote (bFast @ Mar. 12 2008,10:41)
Zachriel, "I am still willing to give him a chance to make his point."

As I mentioned earler, I have modified my sim to log its results, and to do a run, advance, run cycle.  I am also running a pure-random baseline, so that we can see exactly what genetic drift will do.  When I have a package of serious data, then there will be results to talk about.

Does that mean you'll be interested in discussing the real sequence data too?
Quote
I have placed one question before you all that I haven't had an answer to yet.

That's not true, bFast. I was completely forthcoming and answered it as completely as possible.
Quote
How many alleles are there in the human, or another mammal's, population that directly affect the phenotype.

I answered, "I don't know, but I know that each of us is heterozygous for 5-10 recessive lethal alleles. Does that help? The other place to look is in the huge study of Icelandic folks, which would only provide a lower bound, as they are very inbred."
Quote
What number should I be using for my gene count?

That's a completely different question. You have conflated "allele" with both "version of a protein" and "gene," and neither is correct.
Quote
So far I have numbers from the unbelievably low 250, to a high of 16,000.  However, whether the 16,000 all register a difference in the human phenotype is not clear.

For genes, I would start with dozens and gradually increase until the answer is clear. The real number of genes (30000) seems like too much for your sim to handle.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 12 2008,15:10   

JAM:  
Quote
The other place to look is in the huge study of Icelandic folks, which would only provide a lower bound, as they are very inbred."


I do not have access to the journals.  Is the information on the Icelandic folks published on the net?  

Quote
You have conflated "allele" with both "version of a protein" and "gene," and neither is correct.

I understand that an allele is a version of a gene.  I understand that there are non-coding genes.  I understand that introns, for instance, often affect the phenotype.  I would assume that an intron would be seen as a non-coding gene.  However, I may be incorrect when I assume that an intron would be seen as a gene, or a portion of a gene even though it is not a gene that codes to protein.  Alas, this only goes to the question of exactly how the word "gene" is defined by biologists, not to my understanding of what an allele is.  

Is it safe to say that an allele is a variant of a segment of DNA that acts as a unit, where a coding gene is an example of a segment of DNA that acts as a unit -- translating into protein.

If a gene codes to a protein, as somewhere between 20,000 and 30,000 do, then any two versions of that protein would indicate two versions of the gene, two alleles, would they not?  I agree that I sometimes refer to two versions of proteins because the proteins are closer to the phenotype, and it is only the phenotype that natural selection works on.  However, I do recognize that the "alleles" are the variants of the genes involved.
Quote
For genes, I would start with dozens and gradually increase until the answer is clear. The real number of genes (30000) seems like too much for your sim to handle.

I am starting with 200.  There are surely 200 phenotype affecting alleles in the human population.  My simulator can probably handle about 5,000, maybe 10,000.  However, I think that the range of 200 to 2000 will produce an algebraic curve that will allow for reasonable extrapolation.  

I am of the impression that for most genes there is only one allele, or if there are more, that the other alleles don't affect the phenotype.  If there is only one allele, it doesn't count in my sim, its only the multiple-allele genes, introns, etc., where the two alleles produce differences in the phenotype that should count for my sim.  

Further, when I consider the 6000 disease producing alleles, I assume that they have very low rates in the population.  As I consider this, it becomes clear to me that some reasonable level of "rare allele" can be dismissed.

Quote
For genes, I would ... gradually increase until the answer is clear.


By time I have run my sim, I will have an algebraic expression that follows the curve.  Is that what you mean by "until the answer is clear", or are you suggesting that once I determine the point when natural selection no longer grabs the mutation as proof of how many phenotype affecting alleles the human family has?

  
Wesley R. Elsberry



Posts: 4807
Joined: May 2002

(Permalink) Posted: Mar. 12 2008,16:12   

Quote (bFast @ Mar. 12 2008,10:41)
Zachriel, "I am still willing to give him a chance to make his point."

As I mentioned earler, I have modified my sim to log its results, and to do a run, advance, run cycle.  I am also running a pure-random baseline, so that we can see exactly what genetic drift will do.  When I have a package of serious data, then there will be results to talk about.

Zachriel:    
Quote
I did try to clarify bFast's terminology earlier in the thread in order to fully comprehend what he was trying to claim. However, he hasn't been too forthcoming on answering my questions.


Which question have I not been forthcoming about?

I have placed one question before you all that I haven't had an answer to yet.  How many alleles are there in the human, or another mammal's, population that directly affect the phenotype.  What number should I be using for my gene count?  So far I have numbers from the unbelievably low 250, to a high of 16,000.  However, whether the 16,000 all register a difference in the human phenotype is not clear.

250 was unbelievable because it was premised upon

- the false belief that characterizing the degree of genetic difference between two individuals was also a characterization of total variation in the population from which the individuals were taken

- the false belief that alleles were proteins

- the false belief that each amino acid represented one opportunity for genetic change

- the false belief that each individual carried only one copy of the genetic information

- the false belief that 100 amino acids is an average length of proteins in the proteome

A correction concerning the 250 number followed shortly after it was first posted.

There seems to be some fixation on the 16,000 number, though it was clearly stated that was merely the number of proteins currently annotated in a particular database and not the total number of proteins (or, more precisely, representative proteins) in the human proteome.

   
Quote

The current estimate of the size of the non-redundant proteome is ~23,000 proteins (Ensembl, www.ensembl.org), and at present more than 16,000 of those have been manually annotated by the Swiss-Prot/UniProt effort (www.uniprot.org).


They were only interested in collecting one protein per locus, which  completely blows off the issue of prevalence of alternatives due to allelic variation.

I already pointed out that the 16,000 number wasn't what bFast wanted.

I also pointed out that one could derive an estimate of the minimum number of alleles in the human population based upon the information in two comments, this one and this one. I get 27,600 on the back on my envelope for that figure.

--------------
"You can't teach an old dogma new tricks." - Dorothy Parker

    
C.J.O'Brien



Posts: 395
Joined: Aug. 2005

(Permalink) Posted: Mar. 12 2008,16:17   

Quote
If a gene codes to a protein, as somewhere between 20,000 and 30,000 do, then any two versions of that protein would indicate two versions of the gene, two alleles, would they not?  I agree that I sometimes refer to two versions of proteins because the proteins are closer to the phenotype, and it is only the phenotype that natural selection works on.  However, I do recognize that the "alleles" are the variants of the genes involved.

Your terminology is still confused. An allele that results in a different sequence of amino acids by definition codes for a different protein, not a different "version" of the same protein. Not being well-versed in biochemistry, I'm not even sure that terminology is ever used, but I suspect that if it is, it refers to the same sequence of amino acids folded differently.

You're still not dealing with the idea of loci, which is the concept underlying alleles as "different versions" of the same gene. We consider them different versions of the same gene because they are two different sequences at exactly the same locus on the same chromosome.

--------------
The is the beauty of being me- anything that any man does I can understand.
--Joe G

  
swbarnes2



Posts: 78
Joined: Mar. 2006

(Permalink) Posted: Mar. 12 2008,16:41   

[quote=bFast,Mar. 12 2008,15:10]
Quote
I understand that there are non-coding genes.


Non-coding gene?  I've never heard the term.  

Sure there are non-coding sequences of DNA that have important functions, but we don't call promotors genes, for instance.  

Can you give us, say, the name of an non-coding gene in any organism?

Quote
I would assume that an intron would be seen as a non-coding gene.  However, I may be incorrect when I assume that an intron would be seen as a gene, or a portion of a gene even though it is not a gene that codes to protein.


You assume wrong.  Introns aren't genes.  They are non-coding parts of genes.

Quote
Alas, this only goes to the question of exactly how the word "gene" is defined by biologists, not to my understanding of what an allele is.


Well, why don't you start there?

Why didn't you start there in the first place?

Quote
Is it safe to say that an allele is a variant of a segment of DNA that acts as a unit, where a coding gene is an example of a segment of DNA that acts as a unit -- translating into protein.


Don't be silly.  The segments of DNA that are transcribed into t-RNAs are certainly called genes.

Quote
If a gene codes to a protein, as somewhere between 20,000 and 30,000 do, then any two versions of that protein would indicate two versions of the gene, two alleles, would they not?


Nope.  You can have different splicing of the same mRNA sequence in eukaryotes.  

Quote
There are surely 200 phenotype affecting alleles in the human population.


There are about that many alleles of the MCH locus, which affects the phenotype of tissue matching.

Quote
However, I do recognize that the "alleles" are the variants of the genes involved.


See, your "200 alleles" phrasing is what's making people think that you don't.

If it were me, I'd be saying "I'm simulating with 100 genes, each of which has 5 alleles", so as to distinghush between simulating with 5 genes of 50 alleles, or 250 genes with 2 alleles.  And I bet almost everyone else on this board would describe the experiment the same way.

Those are all different simulations, and just saying "I'm simulating a genome with X alleles" doesn't say much about the experiment, and suggest that you aren't differentiating between genes and alleles.  

Quote
However, I think that the range of 200 to 2000 will produce an algebraic curve that will allow for reasonable extrapolation.  


Are you relaly talking about that many alleles at only one locus?  One gene?

Simulating 2000 alleles at one gene isn't going to tell you much.  Simulate 5 alleles at 10 genes, with some way to simulate interaction between the gene products, that will be interesting.

  
Albatrossity2



Posts: 2780
Joined: Mar. 2007

(Permalink) Posted: Mar. 12 2008,17:03   

Quote (bFast @ Mar. 11 2008,21:28)
I understand perfectly what an allele is.  You all are just playing the "creationists aren't evolutionists because they don't understand the basics" card.  It is bull!

And of course this is completely unlike the folks on UD and other venues who demand that you read all of the books written by Behe, Dembski and Wells before they will discuss CSI with you.

Sauce for the goose, etc.

Oh, BTW, I am a Ph.D. biologist too, and I am only delurking here to let you know that I find your blustering about biology to be quite hilarious.

Carry on.

--------------
Flesh of the sky, child of the sky, the mind
Has been obligated from the beginning
To create an ordered universe
As the only possible proof of its own inheritance.
                        - Pattiann Rogers

   
jeannot



Posts: 1200
Joined: Jan. 2006

(Permalink) Posted: Mar. 12 2008,17:24   

Quote (swbarnes2 @ Mar. 12 2008,16:41)
[quote=bFast,Mar. 12 2008,15:10]  
Quote
I understand that there are non-coding genes.


Non-coding gene?  I've never heard the term.  

Sure there are non-coding sequences of DNA that have important functions, but we don't call promotors genes, for instance.  

Loci that produce RNAs are non-coding, but are still called "genes". At least, the locus for 16S RNA is referred to as a gene.

Still, I'm not sure what this simulation is about.
It looks like the problem of natural selection in a population has been solved long ago.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 12 2008,17:29   

Gentlemen,

A common definiton of evolution is, "change in allele frequency over time", correct?

Please, gentlemen, hash out between yourselves a comprehensive definition of allele, I will happily use your definition.

  
C.J.O'Brien



Posts: 395
Joined: Aug. 2005

(Permalink) Posted: Mar. 12 2008,17:36   

Why don't you just start using the only definition there is? Don't project your confusion onto us.

--------------
The is the beauty of being me- anything that any man does I can understand.
--Joe G

  
jeannot



Posts: 1200
Joined: Jan. 2006

(Permalink) Posted: Mar. 12 2008,17:49   

Quote (bFast @ Mar. 12 2008,17:29)
Gentlemen,

A common definiton of evolution is, "change in allele frequency over time", correct?

Please, gentlemen, hash out between yourselves a comprehensive definition of allele, I will happily use your definition.

Our discussion over non-coding genes has very little to do with the definition of allele that you could to use.
Take the one provided by wikipedia. It looks good enough.

Technically, alleles are not limited to genes. Microsatellites aren't genes, but they have plenty of alleles.
I would say that an allele is every intraspecific form of a locus produced by a "local" mutation (i.e not a major indel, duplication, chromosomal change... although this could be discussed).

Update:
A broader definition would cover every copy of a locus that exist within a species, but between haploid genomes, considering that a diploid has only 2 haploid genomes (and not 2 genomes per cell).
This broad definition is implicit when you consider that every locus has two alleles in a diploid organism.
In that case, between-cell copies of a locus within an individual are not considered as alleles, neither are the copies carried by the two chromatids produced during replication.

Actually, the definition can be slightly altered for convenience, depending on your problem.

  
swbarnes2



Posts: 78
Joined: Mar. 2006

(Permalink) Posted: Mar. 12 2008,18:19   

[quote=jeannot,Mar. 12 2008,17:24
Quote
Loci that produce RNAs are non-coding


I'll buy that, if that's how people really use the term.  I just never thought of them that way.  Sure, they don't get translated into amino acids, but the data is in the form of DNA, and it get 'encoded' into RNA to be functional.

But, if the definition is indeed that RNA genes don't make the cut, then I stand corrected.

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 12 2008,18:34   

[quote=bFast,Mar. 12 2008,15:10][/quote]
bfast:
Quote
I understand that an allele is a version of a gene.  I understand that there are non-coding genes.  I understand that introns, for instance, often affect the phenotype.

Who wrote this:

"No, I actually mean allele.  An allele is a variant of the same protein.  Somewhere in the genome there is a protein that controls for eye color.  One variant produces blue eyes, the other produces brown eyes.  Likely the allele producing green eyes is a third allele of the same protein. "

Quote

 I would assume that an intron would be seen as a non-coding gene.


No, an intron is part of a gene.
Quote
However, I may be incorrect when I assume that an intron would be seen as a gene, or a portion of a gene even though it is not a gene that codes to protein.


No, an intron is a part of a gene.
Quote
 Alas, this only goes to the question of exactly how the word "gene" is defined by biologists, not to my understanding of what an allele is.  


"No, I actually mean allele.  An allele is a variant of the same protein.  Somewhere in the genome there is a protein that controls for eye color.  One variant produces blue eyes, the other produces brown eyes.  Likely the allele producing green eyes is a third allele of the same protein. "


I don't think it is the biologists that have the problem.

It is the non-biologists that think they can gain google or wiki expertise or read a few creationist books and pontificate on biology on par with actual biologists.

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 12 2008,18:37   

Quote (bFast @ Mar. 12 2008,17:29)

bfast:
Quote
Gentlemen,

A common definiton of evolution is, "change in allele frequency over time", correct?


Yes - not protein, not intron.
Quote

Please, gentlemen, hash out between yourselves a comprehensive definition of allele, I will happily use your definition.

Nice way to cover your ignorance.

Stick to writing scanning software.

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 12 2008,19:11   

Quote (bFast @ Mar. 12 2008,10:41)
Zachriel:  
Quote
I did try to clarify bFast's terminology earlier in the thread in order to fully comprehend what he was trying to claim. However, he hasn't been too forthcoming on answering my questions.


Which question have I not been forthcoming about?

Well, let's start with what I consider the most important question.  

* You claim that some beneficial mutations can be lost in genomes that vary wildly in fitness. So!? This is the expected result.

Allele Blender is still a few days away. But here's a very stripped down version that only does bFast's basic algorithm. You have to set the parameters in the Declarations module of the VBasic editor. Press ctrl-g to cycle through generations.

   ' Parameters
   Public Const maxGenerations As Integer = 1
   Public Const maxGenes As Integer = 20
   Public Const maxRows As Integer = 20
   Public Const maxCols As Integer = 10
   Public Const Mutants As Single = 1 / 20


maxGenes is the number of genes in each genome.
maxRows * maxCols is the population.
Mutants is the proportion of the population born with a single 2-allele.

--------------
Proudly banned three four five times by Uncommon Descent.
There is only one Tard. The Tard is One.

   
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 12 2008,19:24   

Hmmm, no takers on a definition of allele?  Let me try someone else's for you gurus to shoot apart:

Dictionary.com:
Quote
any of several forms of a gene, usually arising through mutation, that are responsible for hereditary variation.


American Heritage Dictionary:
Quote
One member of a pair or series of genes that occupy a specific position on a specific chromosome.


'Seems that every variant of formal definition that I can find on dictionary.com all include "gene" in their definition.  Now, either my definition is plenty right enough, or the 7 dictionaries sited on dictionary.com are all wrong.

Now, ladies and gentlemen, give me a working definition of allele that isn't bickered with, or accept the American Heritage Dictionary's definition.

Honest folks, I think that this thread has meandered into people finding fancy ways of telling other people that they are stupid becuase either you all have narcisistic personality disorder, or because you fear that I have your pet theory by the short hairs.

  
Wesley R. Elsberry



Posts: 4807
Joined: May 2002

(Permalink) Posted: Mar. 12 2008,19:48   

Quote (bFast @ Mar. 12 2008,19:24)
Hmmm, no takers on a definition of allele?  Let me try someone else's for you gurus to shoot apart:

Dictionary.com:  
Quote
any of several forms of a gene, usually arising through mutation, that are responsible for hereditary variation.


American Heritage Dictionary:
Quote
One member of a pair or series of genes that occupy a specific position on a specific chromosome.


'Seems that every variant of formal definition that I can find on dictionary.com all include "gene" in their definition.  Now, either my definition is plenty right enough, or the 7 dictionaries sited on dictionary.com are all wrong.

Now, ladies and gentlemen, give me a working definition of allele that isn't bickered with, or accept the American Heritage Dictionary's definition.

Honest folks, I think that this thread has meandered into people finding fancy ways of telling other people that they are stupid becuase either you all have narcisistic personality disorder, or because you fear that I have your pet theory by the short hairs.

I provided two already. It seems a bit tendentious to claim that things haven't been provided when it is easy to confirm that they exist in the thread.

Perhaps reading what other people write in responses might prove, hmmm, instructive?

--------------
"You can't teach an old dogma new tricks." - Dorothy Parker

    
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 12 2008,20:03   

Wesley R. Elsberry  
Quote
I provided two already.
 The first problem is that you provided two.  I only want one!

I have found no definition of allele on this site that has been provided by you or any one else on this site and approved by the others on this site  I am fed up with this "you don't know what you are talking about" bit.  I want to work with one definition of allele that all of you can agree on.  That will end the bickering about the definition of the term.  Then we might be able to get to a number of how many phenotype affecting alleles there are in a typical population of mammals.  Then I will have a useful number to put into my sim.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 12 2008,20:57   

Let me try again.

If we accept dictionary.com's definiton of allele  
Quote
any of several forms of a gene, usually arising through mutation, that are responsible for hereditary variation.


And if we also accept a very broad definition of gene, such as provided by American Heritage Dictionary:  
Quote
A hereditary unit consisting of a sequence of DNA that occupies a specific location on a chromosome and determines a particular characteristic in an organism. Genes undergo mutation when their DNA sequence changes.


We end up with fairly close to what I have always understood an allele to be:
Quote
any of several forms of a hereditary unit, usually arising through mutation, that are responsible for hereditary variation.

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 12 2008,21:24   

Quote (bFast @ Mar. 12 2008,20:57)
Let me try again.

Tough audience.

Please provide your current algorithm.
Please restate your claim.

--------------
Proudly banned three four five times by Uncommon Descent.
There is only one Tard. The Tard is One.

   
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 12 2008,21:28   

Zachriel:
Quote
Tough audience.

Thank you.

Quote
Please provide your current algorithm.
Please restate your claim.


My dear computer crashed.  I had a memory leak in my dll.  I should get a good spectrum of well summarized results by morning.  (Some of these cycles take half an hour to run, and I'm running about 100 cycles.) I would rather provide my algorithm (slightly modified from the original) and will restate my claim when I post my data.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 12 2008,21:31   

Nope, 50 cycles, 12 are already done, and some of them take less than half an hour.  The worst case, random drift took half an hour.

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Mar. 13 2008,03:49   

Quote (bFast @ Mar. 12 2008,19:24)
you fear that I have your pet theory by the short hairs.

A Nobel awaits then, once you disprove "evolution".

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Wesley R. Elsberry



Posts: 4807
Joined: May 2002

(Permalink) Posted: Mar. 13 2008,05:53   

bFast:

Quote

We end up with fairly close to what I have always understood an allele to be:


The fact is that you provided math that demonstrated vividly that you did *not* always have that understanding.

Either you are continuing with the same erroneous math, indicative of erroneous understanding, or you have adopted more accurate math indicating a difference between your previous understanding and the state you are in now. Anybody can correct personal ignorance. Admitting that one is actually learning from experience is not a bad thing. Failing to admit that, though, is both transparently obvious and annoying.

--------------
"You can't teach an old dogma new tricks." - Dorothy Parker

    
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 13 2008,06:57   

A randomized genome of 0's and 1's with an initial smattering of 2's is not what we would expect. In nature, traits tend to vary as a probability distribution about a mean.

bFast is imposing a contrived situation to match his expectations. But regardless of whether we start with a random distribution or a flat one, if we allow occasional mutations to occur, the population spontaneously evolves towards a mass probability distribution about the mean.

 Genes = 20
 Population = 10000
 Generations = 20
 A sample gene:

 Allele    Count
    0       140
    1      5603
    2      3825
    3       416
    4        16

 mean ~1.46


The result of random mutation in the toy universe resembles (in this one aspect) what we observe in nature. This example only allows 0's, 1's and 2's.

 Genes = 20
 Population = 10000
 Generations = 20
 A sample gene:

 Allele    Count
    0       370
    1      6700
    2      2930

 mean ~1.26


It's a result of historical evolution, not due to anyone's expectations or preconceptions.

--------------
Proudly banned three four five times by Uncommon Descent.
There is only one Tard. The Tard is One.

   
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 13 2008,07:49   

Quote (bFast @ Mar. 12 2008,19:24)
Honest folks, I think that this thread has meandered into people finding fancy ways of telling other people that they are stupid becuase either you all have narcisistic personality disorder, or because you fear that I have your pet theory by the short hairs.

The irony is rich.

The creationist not only projects, but then goes on to engage in the rampant megalomania that seems nearly endemic in those that inhabit protected pro-creationism blogs and forums.


Let us not forget that bfast the computer tech not only claimed that alleles are proteins, but EXPANDED on that theme:


No, I actually mean allele.  An allele is a variant of the same protein.  Somewhere in the genome there is a protein that controls for eye color.  One variant produces blue eyes, the other produces brown eyes.  Likely the allele producing green eyes is a third allele of the same protein.

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 13 2008,07:50   

Quote (bFast @ Mar. 12 2008,20:03)
I am fed up with this "you don't know what you are talking about" bit.

You are fed up with the truth?

Too bad.

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 13 2008,07:51   

Quote (oldmanintheskydidntdoit @ Mar. 13 2008,03:49)
Quote (bFast @ Mar. 12 2008,19:24)
you fear that I have your pet theory by the short hairs.

A Nobel awaits then, once you disprove "evolution".

But, but - Warren Bergerson already did that!

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 13 2008,08:00   

Quote (Zachriel @ Mar. 13 2008,06:57)
bFast is imposing a contrived situation to match his expectations.

Well, of course.

That is what these people do.

I mentioned Warren Bergerson (aka 'LifeEngineer')above - surely most of us remember him?

If not, he is a retired actuary who claimed for years that he had disproved evolution using 'actuarial math.'  And, after years of claiming this, it was drawn out of him, on ARN, that he had in fact never done any calculations at all, he just "knew" that if he had done so, it would have disproved evolution.

After some prodding, he finally revealed his math on Terry Trainor's MSN group, Talkorigins (note that the guy that pointed out Bergerson's stupidity was eventually railroaded and banned - just like what happens at UD).  His claims were challenged, and he ended up changing his formulae and inputs 3 times when shown to be in error (never admitting it, of course), each time coming up with the same answer.  That is, he rigged the formulae repeatedly to get the results he wanted, to include doing a simple probability calculation backwards.

Same thing with this UD denizen.  He's just making it up as he needs it to be.

  
Cedric Katesby



Posts: 55
Joined: Aug. 2006

(Permalink) Posted: Mar. 13 2008,08:35   

bFast, have you read the "Uncommonly Dense" thread at After the Bar Closes?

If so, what do you think of the comments/threads preserved there that UD tried to flush down the memory hole because they got embarrassing?

Are you really comfortable associating with such a crowd?

P.S.
I will say I am surprised that you have ventured out of the echo-chamber.  Good for you.
I hope you'll stay the course and not disappear.

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 13 2008,09:17   

Quote (Cedric Katesby @ Mar. 13 2008,08:35)
bFast, have you read the "Uncommonly Dense" thread at After the Bar Closes?

If so, what do you think of the comments/threads preserved there that UD tried to flush down the memory hole because they got embarrassing?

Are you really comfortable associating with such a crowd?

P.S.
I will say I am surprised that you have ventured out of the echo-chamber.  Good for you.
I hope you'll stay the course and not disappear.

The Uncommonly Dense thread has a high snark-to-content ratio — which is quite appropriate for the subject matter. However, I would like to keep this thread close to topic. BFast should understand that in an open forum, we have to be somewhat tolerant. My efforts to test bFast's claims should be sufficient evidence of my willingness to consider his views.

I, too, am glad that bFast has ventured outside the cloister. He has yet to be forthcoming in his responses, but I assume that's because he is still attempting to understand how his toy world works.

---------------
* You claim that some beneficial mutations can be lost in genomes that vary wildly in fitness. So!? This is the expected result.

* You claimed that your random genomes of sufficiently large size would not evolve directionally. My results were different. How can you explain this?

* Your randomized population rapidly evolves by sorting through the 0's and 1's of the genome. If we introduce the occasional random mutation, the results tend towards a mass probability distribution (most apparent with a wide variety of available alleles in any given locus). Once some order is imposed, then selection works as expected.

--------------
Proudly banned three four five times by Uncommon Descent.
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dogdidit



Posts: 315
Joined: Mar. 2008

(Permalink) Posted: Mar. 13 2008,11:21   

Quote (Wesley R. Elsberry @ Mar. 12 2008,16:12)
I also pointed out that one could derive an estimate of the minimum number of alleles in the human population based upon the information in two comments, this one and this one. I get 27,600 on the back on my envelope for that figure.

Unlurking here to check my arithmetic:

~23,000 loci in the non-redundant proteome (per HAI abstract)
~20% of those are polymorphic (per Colby's primer)
~6 alleles per polymorphic locus (per...reference?)

yields 27,600 alleles (Dr. Elsberry's number).

And of course it's obvious that this cannot be used in a unitary fashion in the sim(s) under discussion. Seems more sensible to define a proteome with 27,600 loci (if we're doing humans here), 4,600 of which are polymorphic loci with an average of 6 alleles. Nowhere is there a meaningful place to enter "how many alleles in the proteome?".

The next question is, how to model mutation? Is it contrained to the polymorphic loci and only amongst the defined alleles? Seems to me that rules out a lot of novelty.

Apologies to all if my arithmetic is flawed or my terminology and ideas are unschooled (NOT a Bio PhD).

Great thread btw; keep it up! Already on my second bag of popcorn...

*re-engages lurking device*

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"Humans carry plants and animals all over the globe, thus introducing them to places they could never have reached on their own. That certainly increases biodiversity." - D'OL

  
dogdidit



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(Permalink) Posted: Mar. 13 2008,11:36   

I should have said "define a proteome with 23,000 loci" not 27,600. (Dang; post #1 and already he goons it...)

--------------
"Humans carry plants and animals all over the globe, thus introducing them to places they could never have reached on their own. That certainly increases biodiversity." - D'OL

  
Lou FCD



Posts: 5402
Joined: Jan. 2006

(Permalink) Posted: Mar. 13 2008,11:40   



Let's keep this thread on topic, which is bFast's Allele Blender.

I've moved a few comments to the Bathroom Wall that were extraneous.

Quote
Sprinkle on the seat, by Neil T @ Flickr


--------------
Lou FCD is still in school, so we should only count him as a baby biologist. -carlsonjok -deprecated
I think I might love you. Don't tell Deadman -Wolfhound

Work-friendly photography
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bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 13 2008,11:52   

Quote
(oldmanintheskydidntdoit @ Mar. 13 2008,03:49)
Quote
(bFast @ Mar. 12 2008,19:24)
you fear that I have your pet theory by the short hairs.


A Nobel awaits then, once you disprove "evolution".


Oh come on!  There's no chance that a real journal will ever consider these results.  They don't do that.  I don't think this screed at Uncommon Descent is in error.

Zachriel:
Quote
My efforts to test bFast's claims should be sufficient evidence of my willingness to consider his views.


I agree with you Zachriel.  I have interchanged with you on telic thoughts, and in ISCID's brainstorms.  You have always engaged.  I have often criticized UD for kicking you off.  Right now Allan MacNeill is the lone educated voice for the opposition on UD.  He seems to be surviving so far, but UD is rather quick to kick.  

I'd be posting my findings right now, but my computer is bogged down in simulations (around the 800 element array zone) that are taking forever because they are too nearly drifting.  I saw one of the counts get to 750 out of 1000, then meander back down to 0.

As far as mutations ultimately producing a bell curve, that is what I would expect.  Statistically, however, if we are to consider that every gene* that has more than one allele, has exactly two, then 1/2 of the alleles should be 1s and the other half 0s.  That is what we would get if our two alleles per gene* did their best to make a bell curve.  My new sim forces this to be the case for every allele pair but the one under consideration.  It evolves very well with an allele pair count of 200, so my algorithm is not totally flawed.

*As per the American Heritage Dictionary's broad definition.

BTW, I have also been working on a clear representation of my premise, a representation that even slpage should be able to get.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 13 2008,11:57   

dogdidit: [QUOTE]4,600 of which are polymorphic loci with an average of 6 alleles.[QUOTE]

Experts out there, is this a realistic number?  My sim thinks in terms of two alleles per locus.  So my sim should be about correct if it uses 13,800 (4,600 * 6 / 2 ).  Is this about right?

Though my sim currently only considers darwinian death matches, I would think that I should modify it to simulate sexual selection as well.  That will take another 24 hours, but I certainly can do so.

  
Wesley R. Elsberry



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Joined: May 2002

(Permalink) Posted: Mar. 13 2008,12:09   

bFast:

Quote

Experts out there, is this a realistic number?  My sim thinks in terms of two alleles per locus.  So my sim should be about correct if it uses 13,800 (4,600 * 6 / 2 ).  Is this about right?


Ask any statistician whether you can shuffle numbers like that and still have the same variance.

--------------
"You can't teach an old dogma new tricks." - Dorothy Parker

    
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 13 2008,13:53   

Quote (bFast @ Mar. 13 2008,11:52)
Oh come on!  There's no chance that a real journal will ever consider these results.  They don't do that.  

Why would a real journal consider this amateurish pulp fiction?

You could try ISCID I suppose - they are hurting for pro-ID 'science'...

  
JohnW



Posts: 2767
Joined: Aug. 2006

(Permalink) Posted: Mar. 13 2008,14:12   

Quote (Wesley R. Elsberry @ Mar. 13 2008,10:09)
bFast:

Quote

Experts out there, is this a realistic number?  My sim thinks in terms of two alleles per locus.  So my sim should be about correct if it uses 13,800 (4,600 * 6 / 2 ).  Is this about right?


Ask any statistician whether you can shuffle numbers like that and still have the same variance.

Hint:  No.

--------------
Math is just a language of reality. Its a waste of time to know it. - Robert Byers

There isn't any probability that the letter d is in the word "mathematics"...  The correct answer would be "not even 0" - JoeG

  
JAM



Posts: 517
Joined: July 2007

(Permalink) Posted: Mar. 13 2008,15:32   

Quote (bFast @ Mar. 13 2008,11:57)
Experts out there, is this a realistic number?

Yes.
Quote
 My sim thinks in terms of two alleles per locus.  So my sim should be about correct if it uses 13,800 (4,600 * 6 / 2 ).  Is this about right?

Not even close. You can't redistribute that way, as your model is recursive.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 13 2008,15:38   

Wesley R. Elsberry:        
Quote
bFast:

     
Quote

Experts out there, is this a realistic number?  My sim thinks in terms of two alleles per locus.  So my sim should be about correct if it uses 13,800 (4,600 * 6 / 2 ).  Is this about right?

Ask any statistician whether you can shuffle numbers like that and still have the same variance.

Ok, hot shot, rather than suggesting the negitive, suggest the positive.  WHAT NUMBER SHOULD I USE?

C'Mon Dr. Elsberry, stick your neck out a little.  
- Rather than providing a single definition of allele that your buddies can shoot down, you provide multiple definitions -- more accurately multiple explanations of why my definition is wrong.  
- You have failed to provide a number for my sim, even though I have provided the algorithm that I am using.  Instead you shot down five other numbers that were provided by others, each time explaining that their definitions were confused (dispite that some of them hold Ph.D.'s also.)
- Now I take a number, provide a simple algorithmic conversion to fit my sim, and you declare that my calculation is wrong -- but you don't suggest a correct calculation.  

I dare you to provide a positive perspective: a clear, positive (not what it isn't but what it is) definition of allele, a positive number for what value I should use in my sim -- just a series of digits, no hedging, or a positive formula to convert the number that dogdidit provided.  I think you are afraid to provide positive numbers because you think your peers will shoot holes in your positive opinion.

As it turns out I do have a long lost statistician friend.  I'm going to see if I can re-ignite a 10 years lost relationship to get a statistician's opinion on the matter.  My bet is that my number is a rather reasonable approximation, especially since the number is an order of magnitude higher than I need to prove my point.

  
Wesley R. Elsberry



Posts: 4807
Joined: May 2002

(Permalink) Posted: Mar. 13 2008,16:19   

bFast:

If you want a rigorous, technical definition of "allele", I'd suggest going to a textbook on the topic. I provided an abbreviated reference in one of the definitions I quoted earlier. Here's the expanded reference, easily found by looking for the full t.o. jargon file:

Suzuki, Griffiths, Miller and Lewontin. 1989. An Introduction to Genetic Analysis, 4th Edition.

If you want to simulate the specifics of allelic variation, I'd suggest learning about genetic representations, then develop the software requirements and specification documents from that, rather than trying to shoehorn odd bits of biological trivia into an obvious toy simulator at hand.

I've already pointed out that complete analytic solutions already exist for several of the issues that you are interested in and where to find them. You don't need a simulator for most of what you are trying to figure out; evolutionary biologists have already developed closed-form equations for various and sundry issues concerning selection and drift of alleles.

But I don't have a specific, firm, and accurate number that expresses for the human population the total number of polymorphic loci and the variation in numbers of alleles at those loci. Nor do I intend to spend my time doing the literature search that would be necessary to characterize those numbers beyond the small amount I already did earlier in the thread. I have suggested that an estimate of a minimum number of total alleles can be had, and provided that raw number.

The best I can do for you is to do as I have done, and tell you when what you have presented has problems. This is what happens in peer-review; didn't you know that? Peer-reviewers aren't called upon to do the work that an author has failed to do. They are called upon to expose weaknesses and suggest areas for improvement in the work that is submitted. You should consider yourself lucky to have so many talented people willing to do this for you in this informal setting. Yes, you also get to take some intellectual lumps along with that, but that's a hazard of a truly open forum.

--------------
"You can't teach an old dogma new tricks." - Dorothy Parker

    
JohnW



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Joined: Aug. 2006

(Permalink) Posted: Mar. 13 2008,16:39   

Wesley has dealt with the genetics.  Now for the statistics: you're assuming that you can model the behaviour of N loci with many alleles by using a higher number of loci with fewer alleles.  This is incorrect; the distributions are going to be dramatically different.  I think doing is more helpful than telling, so I suggest you try this yourself: it's very easy to put together an Excel spreadsheet (or whatever) comparing, say, a uniform random variable with range 0-6 with the sum of six random binary numbers.  Do this a few hundred times and look at the distributions.  The means will be the same, but not the frequency histograms.

If your simulation won't accommodate more than two alleles, you're going to have to write a better one.

--------------
Math is just a language of reality. Its a waste of time to know it. - Robert Byers

There isn't any probability that the letter d is in the word "mathematics"...  The correct answer would be "not even 0" - JoeG

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 13 2008,17:00   

How do I best explain the issue that I am attempting to simulate.  

Consider that when I was born I had two phenotype-affecting mutations -- oh, by the way, I lived a thousand years ago, before the age of modern medicine.  The first was a mutation that gave me cavity-resistant teeth.  The second gave me a quirky smile.  It would be reasonable to label the first mutation "beneficial".  The second mutation, well, my wife thinks its cute.  Most ignore it.  Some others think its cute, or think its wierd.  One could reasonably label it a neutral mutation.  It affects my phenotype, but in a neither here nor there sort of way.  The first question is, "how much better chance does the beneficial mutation have of fixing in the population than the second has?"

Now, lets consider my beneficial mutation.  I have a friend who had an absessed tooth.  The infection ultimately killed him.  I, with my beneficial mutation am much less likely to die of an absessed tooth.  I also am likely to be able to eat a larger variety of foods because I won't have to gum them as soon.  My less-rotten teeth may even benefit me in the relationship game. There are situations where my beneficial mutation offers me a darwinian benefit.

However, I am a slightly short, stocky man.  I am not nimble on my feet.  I am slightly short-sighted.  I am of slightly above average intelligence.  When I see danger, I tend to freeze rather than flee.  These are only a few of many attributes that are my genetic heretage.  Each one may or may not give me an advantage in a darwinian struggle.  

I was out with a friend once, we bumped into a hornet's nest.  I froze, he ran.  If you know anything about hornets, you know that the go after the moving object.  My friend was stung to death.  I was victorious in that darwinian conflict.  However, I cannot attribute this darwinian victory to the tooth mutation in any way.

Another time I was out with a friend.  This time we came across a cross bear.  I froze, he ran.  The bear didn't buy my play-dead game, and ate me up.  This time the same allele mix that saved my life with the hornets caused my death with the bear.  This point illustrates that many alleles are beneficial in one situation are detrimental in another.  Such alleles, like my quirky smile, are likely to neither dominate nor deteriorate in the population. They are just adrift.  Yet in any darwinian struggle, they are balanced.  They are placed on a continuum from very detrimental to very beneficial.  Most alleles by far, including my dental one, in most darwinian conflict sit in the middle as inconsequential.  Some alleles bounce between beneficial and detrimental.  

If we look at the human population at any time in history, we will notice a near constant number of alleles.  Even though some alleles have moved to fixation, another has been generated to take its place.  So at any time, there is a population of alleles, the predominance of those alleles are "neutral", and any one individual has a near-random mix of those alleles.

Now, there is another major player in the equation of darwinian challenge.  A darwinian challenge is not focused on my genes, it is focused on my entire person.  It is obvious that if I was lucky enough to have been taught how to survive in the woods, I would do better at a "lost in the woods" challenge than my identical twin brother who was never given such training.  But so many of the "darwinian challenges" have a huge random component to them.  For instance, a friend was riding his horse down a well-trodden path.  An avalanch happened and whiped him out.  His genes were removed from the pool, but there was virtually nothing about him that determined this.    Or consider the other side of the table.  Two people are stranded in a cabin during a snowstorm.  One male, one female.  Though these two would likely never connect in a real-world situation, the randomness of the times sees sexual selection take place.  Selected on what?  On randomness.  Therefore, I find it reasonable to include a component of "randomness" to the darwinian equation.

So we come the the second part of the question.  As it is clear that multiple factors are involved in any darwinian challenge (death struggle, or reproductive opportunity) how many factors can natural selection juggle and still positively select for the lucky mutation.  This is the signal to noise problem.  If my lucky mutation was the only thing ever selected for, it would surely dominate the population in no time.  However, every other phenotype affecting allele may, in another challenge, be the more decisive factor.  So if we know how many alleles there are, we know how many other opportunities darwinism has to select for some other factor, rather than the lucky mutation, in any darwinian challenge.  Further, I have included an array of percentages of "random factors" (non-genetic) to factor into the equation.  It is obvious that the more "other factors", the more nearly the lucky mutation's advantage will be minimized.  At what point is its advantage inconsequential?  At what point does random drift have the same effect as the beneficial mutation?

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 13 2008,17:02   

My current algorithm and reasoning is as follows:

term: coin toss - a random number between 0 and 1, 0 = "heads", 1 = "tails".

1: I create an array of array elements.  I initialize each element of the array with a coin toss.  Each number represents two alleles of an organism.  The first element of the array, however, I initialize to 0, and I initialize one random organism to have the first element of 1.  This represents the one lucky mutation.

I then divide my array as follows:
- The first element (lucky mutation) is rated as 0 or 1.
- The subsequent elements are 1/10th the population (- 1 for the last array).  For each segment, I sum up the value in that array and store it.

2: Per cycle, I randomly select two organisms to compete.
- I call a random number < 100,
-   if that number is < "random", I choose the organism that dies by random coin toss.
-   Otherwise I compete them as follows:
-      for element 2 through 10, I call a coin toss.  If heads, I add the fitness of the element for each organism into separate accumulators.  If tails, I subtract the fitness.
-      I add the fitness of element 1 into the accumulator.
-      The organism with the lowest accumulator value is destroyed.
-   I then choose two organisms at random to "mate".  (I could modify my algorithm here to simulate sexual selection.)
-   To mate an organism, I coin toss for each entry in the two organism's arrays, creating a new array.  I then map the strength of each element as described during initialization.
-   I dynamically maintain a count of how many "mutants" are in the array.

3 - Per generation, I run cycles * population.  This will produce an average of 1 death per organism.

4 - I run each level until the mutant has fixed 10 times.  I report the average number of purge events that happen, and the average number of generations until the mutant is fixed.

5 - To provide a baseline, I ran as per 4, but with all organism selection being random.  This represents the effect of genetic drift.

Now, why would I measure the fitness of the two organisms effectively as "random" + the fitness of the mutation of interest?  
1 - IT WORKS!  When I run this using 200 allele pairs, it evolves quite nicely.
2 - If a snapshot of the human population were taken now or at any point in the past, the average number of alleles in the population would remain mostly constant.  Over many generations, I am sure there would be an increase, however, by competing all elements of the array, the exact opposite happens -- there is a decrease in the number of alleles in the population as individual allele pairs fix/purge.  As such, by following my orignial algorithm, I was working in an environment of decreasing noise.  It was quite obvious -- the rate of evolution would increase as fixation happened and the noise reduced.  Seeing as in the real world, the number of alleles increases rather than decreases, I think this approach is fair.  Further, whether in sexual selection or fatal selection, an allele that gives advantage in one situation will be a clear disadvantage in another.  By far the majority of the alleles in the population are drifting, rather than directional.

What types of noise am I now testing and not testing?:

1 - Allele populations.  I am directly testing how the number of alleles in a population affects the lucky mutation's ability to evolve.

2 - The fickleness of natural selection.  The "random" component addresses the fickleness of natural selection.  Further, the toggling of the value addresses (with some exaggeration, admittedly) the ficklenss of natural selection on the alleles not under test.  That said, I am still drastically undervaluing the fickleness of natural selection for the lucky mutation because the lucky mutation is seen as having a positive effect on all non-random events.  My lucky tooth would have a large positive effect in a few situations, but would have no positive effect at all in the vast majority of darwinian challenges.

3 - New alleles are not directly addressed.  However, new alleles are factored in quite reasonably by causing all alleles but the select one to drift.

4 - Bulk editing -- not addressed.

5 - Dominant/recessive genes -- not addressed.

6 - Multiple alleles for the same gene.  This is not addressed by the sim.  However, it produces as many challenges as it does advantages for evolutionary theory.  If the lucky mutation happens to enhance a gene that is not currently very highly rated, it is highly likely that the gene will still by rated below par.  For example, if the lucky mutation happens in an allele that makes the creature less intelligent, the new allele will probably make the creature less intelligent.  In such as scenerio the lucky mutation may well not be selected simply because it is in a bad neighborhood.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 13 2008,17:15   

The data.

I ran each test below until I had 10 fixation events.  The numbers represent:
1 - Percent of random kills.
2 - average number of purged mutations per fixed mutation.
3 - average number of generations until the mutation fixed.

I intended to run through an array size of 1000, but it began to take long enough to get rediculous.  To get data today, I gave up.

The comma delimited data below can be cut and pasted into a text file with the file extension .csv.  They can then be opened with excel, and viewed more elegantly.

Drift, a baseline.
100,915.1,935.9

Array size: 200
Random %,# Purged,Generations til fixed
0,53,367.6
20,39.4,418.4
40,84.1,438.9
60,117.4,510.9
80,306.4,988.2

Array size: 300
Random %,# Purged,Generations til fixed
0,61.7,338.6
20,85.2,427.5
40,146.9,504.6
60,174.6,596.5
80,179.2,824.2

Array size: 400
Random %,# Purged,Generations til fixed
0,96.7,456.4
20,236.6,486.8
40,99.5,698.7
60,167.9,840.6
80,654.6,919.1

Array size: 500
Random %,# Purged,Generations til fixed
0,166.9,427.7
20,84,572.8
40,183.1,665.9
60,321.2,732.7
80,329.7,1012.5

Array size: 600
Random %,# Purged,Generations til fixed
0,82.1,550
20,178.9,745.3
40,208.9,690.4
60,390.1,666.4
80,410.8,977

Array size: 700
Random %,# Purged,Generations til fixed
0,97.1,587.2
20,148.6,671
40,188.7,855.2
60,180.8,815.1
80,354.8,856.3

Array size: 800
Random %,# Purged,Generations til fixed
0,231.2,670.7
20,230.8,620.5
40,247.9,761.7
60,358.5,786.7
80,1100.8,1403.9

Array size: 900
Random %,# Purged,Generations til fixed
0,188.6,827.7
20,185.5,720.2
40,632,1054.7

To summarize what I see in these results.  As the array size increases, the numbers clearly move towards fixation.  As the amount of randomness increases there is a clear move towards fixation.  There are point in this run which are slower than fixation:  800 * 80%, 900 * 40% etc.  

The variance in the results here are still quite dissappointing.  It is clear that I need to run more than 10 cycles to get a good average number.  However, this is a system hog.  In a week I will have better numbers to answer the ultimate question -- at what point is it reasonable to conclude that the lucky mutation has little more chance than random.  Even in this chart, however, we see that without a "random" component, by 900 allele pairs, we have about 1 chance in 200 of our lucky mutation fixing.

  
bFast



Posts: 44
Joined: Mar. 2008

(Permalink) Posted: Mar. 13 2008,17:17   

The next question I see is what where do I need to take this next.

1 - Running each cycle 10 times still leaves a lot of variance.  I need to run each cycle 50 times.  However, it took about 24 hours to run this one, so running 50 times will take about a week.

2 - At least with this crowd I think I need to add sexual selection on top of death selection.  

3 - I need to run a pattern on population size.  I need to see if the results are more attractive, or less attractive as the population increases.  This is really going to slow down the processing.

  
swbarnes2



Posts: 78
Joined: Mar. 2006

(Permalink) Posted: Mar. 13 2008,18:24   

Quote (bFast @ Mar. 13 2008,17:00)
If we look at the human population at any time in history, we will notice a near constant number of alleles.


How did you determine this?

A near constant number of genes, sure, that make sense, but alleles?  It's fairly well accepted that humanity went through a pretty severe bottleneck at one point, how can you be so sure that the allele diversity didn't take a significant nosedive at that point?

As for the rest of the post, whom exactly do you think doesn't know all that?

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 13 2008,18:58   

Quote (bFast @ Mar. 13 2008,17:02)
My current algorithm and reasoning is as follows:

I have no idea what you are doing. What happened to the 2-allele? Are considering only the first gene, which is normally a 0, but once in a population a 1? What's 1/10th the population? I don't get it.

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There is only one Tard. The Tard is One.

   
swbarnes2



Posts: 78
Joined: Mar. 2006

(Permalink) Posted: Mar. 13 2008,19:20   

Quote (Zachriel @ Mar. 13 2008,18:58)
 
Quote (bFast @ Mar. 13 2008,17:02)
My current algorithm and reasoning is as follows:

I have no idea what you are doing. What happened to the 2-allele? Are considering only the first gene, which is normally a 0, but once in a population a 1? What's 1/10th the population? I don't get it.

It's not a well written description.

I think he's got 10 genes, each gene has an allelic value between one and zero.  Does that mean only 1 and 0, or does that means fractions?  I can't tell.  The use of the term "coin flip" to describe generating the latter is indeed odd, but using the term "between" 1 and 0, when you mean 1 and 0 is also odd.  But how else do you fit hundreds of alleles into this sim, without increasing the number of genes?

bfast seems to be perterbed that the overall number of alleles decreases, but without mutation to make new ones, this is completely expected.

He also seems quite sure that because his algorithm is giving him the answers he expects, that this proves that it is both working just as he wants it, and that it is actually doing something productive.  Anyone else think that confidence is premature?

  
Zachriel



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(Permalink) Posted: Mar. 13 2008,21:05   

Consider a very simple case with three genes and a population of three, using bFast's earlier algorithm.

 1) 010
 2) 000
 3) 101


3) competes with 1) winning. 3) combines with 2) to make x0x replacing 1).

 1) x0x
 2) 000
 3) 101


The 1-allele in the second gene is now extinct, even though it is clearly of significant benefit. It doesn't require running a simulation for a week to determine that the Law of Small Numbers applies.

Added:  The lost allele represents a full third of the possible fitness of any sequence, half of any extant sequence. Yet even in a small genome, it's lost in the shuffle.

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bFast



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(Permalink) Posted: Mar. 13 2008,21:06   

Zachriel,"Are considering only the first gene, which is normally a 0, but once in a population a 1?"
Rather than have a gene with two alleles getting the lucky mutation, I am starting with a gene with one allele, allele 0, getting a lucky mutation to make it an allele 1.

Zachriel, "What's 1/10th the population? I don't get it."
The results are an average of ten runs.  Ie, I count the total number of purges during the process of obtaining ten fixes, then I divide that number by 10 to get the average # of purges per fixation.  By the same token, I add up the total number of generations for the ten fixations (only counting the successful fixations of course), then I divide by 10 to get the average number of generations per fixation.


swbarnes2, "I think he's got 10 genes, each gene has an allelic value between one and zero."

No.  The number 10 is the number of times fixation happens during each cycle.  A cycle is a gene count crossed with a random %.  I am initially considering a creature with 200, 2 allele genes.  After running through various levels of "random" input, I consider a creature with 300, and so forth.

I am absolutely limiting myself to integer arithmetic during processing.  A "coin flip" produces a 0 or a 1.

Sorry for a less than clear description.  However, I am please that you guys are seriously looking at my numbers and trying to understand them.  I'll do my best to clarify.

  
Zachriel



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(Permalink) Posted: Mar. 13 2008,21:17   

I'm not up to statistics yet, because I have no idea what the statistics might mean.

* We have a population of sequences.
* Each sequence is composed of 0's and 1's.
* The fitness is the sum of the 0's and 1's.
* The initial sequences are randomized.

Is this correct?

By your old rules, you took two sequences at random, and compared their fitness. The weakest dies. The replacement is a recombination of two sequences at random.

Is that still correct?

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swbarnes2



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(Permalink) Posted: Mar. 13 2008,23:27   

Quote (bFast @ Mar. 13 2008,21:06)
No.  The number 10 is the number of times fixation happens during each cycle.  A cycle is a gene count crossed with a random %.  I am initially considering a creature with 200, 2 allele genes.  After running through various levels of "random" input, I consider a creature with 300, and so forth.


You said in a cycle you look at elements 2-10.  How can an element then be the result of a cycle?

As to what will happen with more genes, I think your simualtion will cause the 1 allele at the first position to be even stronger.

If this:"If heads, I add the fitness of the element for each organism into separate accumulators.  If tails, I subtract the fitness."

Means that for each of your 200 genes, you either add or subtract the 1 or 0 (how else are you measuring the fitness of the element otherwise?  What is an "element anyway?) then your sum, as the number of genes increases will be more and more likely to be 0.  Making the 1 in the first gene, which is always added, and never subtracted, the deciding gene.

I don't think that this has a bit of bearing with regard to what real organisms go through.

  
bFast



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(Permalink) Posted: Mar. 13 2008,23:42   

Zachriel, "By your old rules, you took two sequences at random, and compared their fitness. The weakest dies."  Is that still correct?"

Not really.  

Now, let me reiterate my reasoning.  The allele set in me, and in a typical Australian aboriginal is nearly identical, right?  Yet the Australian aboriginals separated from the rest of mankind about 50 million years ago, only to be rediscovered about 2 to 3 hundred years ago.  If they have a very similar allele set to my own, then the phenomenon of alleles floating around, drifting, far outweighs the phenomenon of alleles fixing.  (I assume that when this was being discussed, we weren't discussing genes that only have one allele.)  If these alleles are just floating around, there can only be two reasons that I can see.  One is that the alleles don't actually affect the phenotype in a way that is ever selected for. As such they should not be in my long saught-after count of alleles.  Or, they are sometimes beneficial, and other times harmful enough that their benefit in one experience is balanced by their harm in another.

If I assume that the average allele is the latter, sometimes beneficial, sometimes harmful, I can simulate this by competing the allele from an element in the first organism, with the allele from the same element in the second, then anti-competing these elements on another occasion.  This is exactly what I have chosen to do.  However, how I am doing this, totally for software performance reasons, is that I am grouping the elements into 10 groups, and either competing or anti-competing them based upon a coin toss.  The result is that all alleles except the one being considered are randomly drifting.

The net effect of this, in fact, is that I may as well be taking a random number to represent competing organism 1, and a random number representing competing organism 2, then if either organism has the lucky mutation, incrementing its number by 1, then doing the standard comparison.

I know that this is a little strange -- even off beat.  However, all I am doing in actuality is changing the texture of the noise that the signal is compared to.  With this somewhat unorthodox move, I have removed the problem that the earlier algorithm was having that as other alleles fixed, they reduced the amount of noise I was analyzing.  As such they were dynamically changing the volume of something that I was trying to measure.

The bottom line of this is that it works!  When I compare my population at 200 allele pairs, evolution happens quite nicely.  As I increase my allele count, evolution continues to happen, but the pace of evolution slows down, becomes more like genetic drift.  Once I get to 900 allele pairs and no noise, I have moved from 50 purges per fixation to about 200 purges per fixation.  The pace of evolution (generations until fixation) has become all but equil to random drift.

At that point, with no "random noise component", we still are beating drift.  It is still taking 900 purges per fixation in the drift.  However at 800 allele pairs, and 80% random, my small test implies that we are beyond drift.  

Of course we will never get beyond drift, but that's part of why I am re-running the thing at 50 cycles per report, rather than 10, just to get tighter averages.  (I also want to be able to see what kind of curve we are getting.  Is it linear?  Probably not, as the allele count increases, the pace at which we approach drift must slow.  I definitely need more precise data to trace such a curve.)  I have also extended the algorithm to add simple sexual selection (organism A mates with the best of Organism B or C.)  In addition, my next test will be in a population of 500, just because I don't want to wait a literal week to get results.

I will be running a test that increases population as it runs to see the effects.  Though I expect that the larger the population, the more difference there will be between drift and any allele pair count, I also expect that the number of purges will go up in all cases.  I just expect that the purge rate will go up faster the closer we get to drift.

  
bFast



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(Permalink) Posted: Mar. 13 2008,23:48   

swbarnes2, the issue of 2-10 has to do with how I am grouping my allele pair array elements to come to a "rating".  I hope that if you read my previous post to Zachriel, my rating system will become more clear.  I will admit it is a bit unorthodox.

As far as, "As to what will happen with more genes, I think your simualtion will cause the 1 allele at the first position to be even stronger."

My premise is exactly the opposite, as more alleles are added, the effect of any one allele should become weaker.  As we get to the number of alleles in a real-world population, the I contend that the effect of any one beneficial mutation will be effectively zero, that the mutation will almost exactly trace expectations of a "neutral" mutation.

  
Bob O'H



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(Permalink) Posted: Mar. 14 2008,01:44   

Quote
2: Per cycle, I randomly select two organisms to compete.
- I call a random number < 100,
-   if that number is < "random", I choose the organism that dies by random coin toss.
-   Otherwise I compete them as follows:
-      for element 2 through 10, I call a coin toss.  If heads, I add the fitness of the element for each organism into separate accumulators.  If tails, I subtract the fitness.
-      I add the fitness of element 1 into the accumulator.
-      The organism with the lowest accumulator value is destroyed.
-   I then choose two organisms at random to "mate".  (I could modify my algorithm here to simulate sexual selection.)
-   To mate an organism, I coin toss for each entry in the two organism's arrays, creating a new array.  I then map the strength of each element as described during initialization.
-   I dynamically maintain a count of how many "mutants" are in the array.

This is needlessly complicated.  Why not simply choose an organism to die, according to its fitness (you can use rejection sampling, which should be quick), and then choose the 2 parents randomly.

I'm surprised you're complaining about it taking a long time.  There shouldn't be anything particularly complicated to simulate.

I'm also with Wes in saying that you're looking at issues that have been sorted out.  There's nothing wrong with trying to replicate them, as it should help you understand evolutionary biology, but don't expect us to be wowed by something new!

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It is fun to dip into the various threads to watch cluelessness at work in the hands of the confident exponent. - Soapy Sam (so say we all)

   
Alan Fox



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(Permalink) Posted: Mar. 14 2008,04:08   

Quote
Yet the Australian aboriginals separated from the rest of mankind about 50 million years ago


???

I take it you meant "thousand", Bruce?

  
Zachriel



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Joined: Sep. 2006

(Permalink) Posted: Mar. 14 2008,07:07   

Quote (bFast @ Mar. 13 2008,23:42)
The allele set in me, and in a typical Australian aboriginal is nearly identical, right?  Yet the Australian aboriginals separated from the rest of mankind about 50 million years ago, only to be rediscovered about 2 to 3 hundred years ago.  

I don't think they knew they were lost.

Anyway, it's only been a few tens of thousands of years. There are certainly some regional differences, but many variations are inherited from the common population. Other variations have become fixed, mostly due to the founder effect (drift). While still others were added to the population by mutation.

Quote (bFast @ Mar. 13 2008,23:42)
One is that the alleles don't actually affect the phenotype in a way that is ever selected for. As such they should not be in my long saught-after count of alleles.  Or, they are sometimes beneficial, and other times harmful enough that their benefit in one experience is balanced by their harm in another.

Or perhaps the mixture itself is subject to group selection, that a varied group is beneficial to each member of the community. What I call Seven Dwarves Selection: Dopey, Grumpy, Doc, Happy, Bashful, Sneezy, Sleepy.

Quote (bFast @ Mar. 13 2008,23:42)
However, how I am doing this, totally for software performance reasons, is that I am grouping the elements into 10 groups, and either competing or anti-competing them based upon a coin toss.  The result is that all alleles except the one being considered are randomly drifting.

In other words you abandoned your previous algorithm. So much for Allele Blender. And needlessly complicated.

You have every selection coeffecient oscillating between the discrete values of +1 and -1. I just don't know why you are doing this.

Quote (bFast @ Mar. 13 2008,23:42)
With this somewhat unorthodox move, I have removed the problem that the earlier algorithm was having that as other alleles fixed, they reduced the amount of noise I was analyzing.  As such they were dynamically changing the volume of something that I was trying to measure.

You're wasting a lot of time by not thinking your simulation through before implementing the code. It's clear you have a result in mind and that you haven't read anyone's responses on this thread.

You appear to have abandoned your original model because it didn't show what you wanted it to. Perhaps it was trying to tell you something.

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Reciprocating Bill



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(Permalink) Posted: Mar. 14 2008,07:08   

bfast -

The notion that your original assignment of 0s and 1s to each locus models alleles with relative degrees of fitness is obliterated by your application of an additional coin toss at the time of "competition" that determines whether the allele at each position will be added or subtracted from the total.  

Alleles of 0 never impact the total fitness score. Hence your original assignment of 1s and 0s determines only which loci will participate in determining the totals during competitions, not the relative fitness of the alleles present at those locations.

No relative degree of "fitness" is denoted by an assignment of 1 because the competition-time coin-flip is tantamount to the assignment of a "sign" that wholly determines that location's fitness contribution. No selection related to fitness occurs, either, because that sign is subsequently discarded even if the organism survives.

Nor does the outcome of "mating" do anything other than determine, again, how many locations will participate in the determining the total (as those containing zeros drop out), not the fitness of the resulting organism.

Lastly, your notion that an assignment of a "lucky 1" represents a gift of extra fitness is mistaken. Because values at other positions do not determine fitness of the allele, but merely participation in determining the total, your lucky 1 does not model a gift of extra fitness - rather, it confers guaranteed participation, only. But even that is lost, because  your lucky 1 is not subject to the assignment of a sign at competition time, and doesn't participate in the process in the same manner as the other loci. So it is far from analogous to a gift mutation. Your assignment of a "lucky 1" to one position of one organism could be accomplished just as easily by intializing the "accumulator" of that organism at 1 rather than 0 prior to each competition. You've just put your thumb on the scale for that organism, not conferred extra fitness.

In short, all you are "modeling" with all this machinery are probabilities that a random coin flip at N locations (N=the number of loci originally assigned a value of 1) will yield more than 1/2N + 1 heads, and thereby survive in competition against the lucky organism. (Add to that the likelihood that the lucky organism will yield fewer heads as signs are assigned). We can do a little binomial math to determine those probabilities. NOTHING going on here resembles natural selection, evolution, etc.

(Programming note: I'd initialize your data structure as a 2-dimensional array, with one subscript denoting organism and the second denoting gene-locus. Probably would be a lot easier to manipulate).

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"Here’s a clue. Snarky banalities are not a substitute for saying something intelligent. Write that down."
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Zachriel



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(Permalink) Posted: Mar. 14 2008,07:19   

Quote (Zachriel @ Mar. 14 2008,07:07)
You appear to have abandoned your original model because it didn't show what you wanted it to. Perhaps it was trying to tell you something.


We already know that beneficial genetic variations can be lost due to the Law of Small Numbers.

* You claim that some beneficial mutations can be lost in genomes that vary wildly in fitness. So!? This is the expected result.

* Novel variation is due to genetic mutation. We can observe this process in nature, and a slightly modified version of your original program demonstrates the point. It's *not* something that has to be imposed by the programmer.

The goal isn't to prove that a particular system works the way you think it should. (Notice that all I did was  take your original model and add random mutation. The result was an evolving system which had highly individualized sequences, natural variations spread across a mean, and increasing fitness.)

You need to be able generalize your results to include a sufficiently large class of evolutionary algorithms so that it might reasonably shed light on the behavior of biological systems. To do so would seemingly require simplicity, not complexity.

I think your simulation is flawed, but it's hard to tell as I still don't know what it does exactly.


Quote (Reciprocating Bill @ Mar. 14 2008,07:08)
The notion that your original assignment of 0s and 1s to each locus models alleles with relative degrees of fitness is obliterated by your application of an additional coin toss at the time of "competition" that determines whether the allele at each position will be added or subtracted from the total.

That's what I thought he said.

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dogdidit



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(Permalink) Posted: Mar. 14 2008,10:19   

This assumption is at the core of bFast's sim:
   
Quote (bFast @ Mar. 13 2008,17:00)

[...] This point illustrates that many alleles are beneficial in one situation are detrimental in another.  Such alleles, like my quirky smile, are likely to neither dominate nor deteriorate in the population. They are just adrift.  Yet in any darwinian struggle, they are balanced.  They are placed on a continuum from very detrimental to very beneficial.  Most alleles by far, including my dental one, in most darwinian conflict sit in the middle as inconsequential.  Some alleles bounce between beneficial and detrimental.  

Thus no allele positively contributes to fitness in all survival situations ("darwinian conflicts"??) except for the "1" allele at the first locus of the genotype of the one lucky organism in the colony. The rest either oscillate back and forth in fitness value or play no role at all.

This might make sense if he were trying to simulate the varying pressures of the environment, and how changing conditions modulate the survival value of phenotypic differences. But then ALL the members of the colony should be simultaneously encoutering the same environmental pressures (I'm thinking of the Grant's study of the Galapagos finches, my familiarity with which coming entirely from Joseph Weiner's book). Instead the environment in his sim is entirely chaotic - sometimes hornets, sometimes bears.

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bFast



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(Permalink) Posted: Mar. 14 2008,10:24   

Allan Fox, "I take it you meant "thousand", Bruce?"  Yup.  Thanks for the correction.

Reciprocating Bill, you seem to be suggesting that my algorithm shouldn't work at all. Right?  Well, evolution happens in it at the 200 allele point quite nicely, so it obvously works, at all.  

About the 0 and 1, its exactly mathematically the same as labeling them 1 and 2, honest.

Zachriel,
Quote
You're wasting a lot of time by not thinking your simulation through before implementing the code.
 There is truth in this statement.  This is my first forey deep into the territory of an evolution simulator (where I've run it through gobs of cycles.)  It is a learning experience which is affecting my algorithm.

Quote
It's clear you have a result in mind and that you haven't read anyone's responses on this thread.

You appear to have abandoned your original model because it didn't show what you wanted it to. Perhaps it was trying to tell you something.

Not so much.  I am trying actually to eliminate reporting challenegs.  If 50% of the alleles have fixed by time my lucky allele also fixes, the amount of noise that my allele is facing is significant.

I have pondered this challenge.  How do I sensibly return the algorithm to the original.  In this thought, it has dawned on me that I should return to the orignal measure of fitness, and at the end of a successful fixing, I should count the number of 1s that have fixed and the number of 0s that have fixed.  If the whole system is drifting, the fixed 1s and the fixed 0s should be about equil.  

This may be a more sensitive measure of whether the thing is still evolving than the two measures I am currently using -- number of purges per fixation, and number of generations til fixation.  You will note that I initially was only using the latter number, and I was seeding the generator with 100 identical mutations to reduce the purge rate.  However, the "# of generations" measure shows that in some cases I have fully reached drift, but my purge rate count is slower to show the same thing.

  
swbarnes2



Posts: 78
Joined: Mar. 2006

(Permalink) Posted: Mar. 14 2008,11:49   

Quote (bFast @ Mar. 14 2008,10:24)
Reciprocating Bill, you seem to be suggesting that my algorithm shouldn't work at all. Right?


No, he's not.

He's saying that the mathematical contortions you are going through don't have any connection to evolution.

And he's hardly alone in that assessment.

 
Quote
Well, evolution happens in it at the 200 allele point quite nicely, so it obvously works, at all.  


No, it's not obvious.  Just because you get the answer you expect doesn't mean that the program is working the way you think it is, or that what you intend it to do is meaningful.



 
Quote
This is my first forey deep into the territory of an evolution simulator (where I've run it through gobs of cycles.)  It is a learning experience which is affecting my algorithm.


Your program isn't simulating evolution very well.  Its' telling you that 1 + the sum of a lot of random 1's -1's, and 0's is usually larger than the sum of 1's, -1's, and 0's.

You don't need hours of computer time to tell you that.

<edited typo>

  
Reciprocating Bill



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(Permalink) Posted: Mar. 14 2008,13:29   

Quote (swbarnes2 @ Mar. 14 2008,12:49)
Quote (bFast @ Mar. 14 2008,10:24)
Reciprocating Bill, you seem to be suggesting that my algorithm shouldn't work at all. Right?


No, he's not.

He's saying that the mathematical contortions you are going through don't have any connection to evolution.

Exactly. More anon.

--------------
Myth: Something that never was true, and always will be.

"The truth will set you free. But not until it is finished with you."
- David Foster Wallace

"Here’s a clue. Snarky banalities are not a substitute for saying something intelligent. Write that down."
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swbarnes2



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(Permalink) Posted: Mar. 14 2008,14:33   

Quote (bFast @ Mar. 13 2008,23:42)
The allele set in me, and in a typical Australian aboriginal is nearly identical, right?


What was the point of getting into a snit about how no one would give you hard numbers about human genetic diversity, when you were going to just assume what you wanted regardless?

 
Quote
If they have a very similar allele set to my own, then the phenomenon of alleles floating around, drifting, far outweighs the phenomenon of alleles fixing.


How on earth do you conclude this?

If you think that you are mostly identical to an Aboriginal, doesn't that mean that those alleles you have in common are fixed in the whole human population?

 
Quote
One is that the alleles don't actually affect the phenotype in a way that is ever selected for. As such they should not be in my long sought-after count of alleles


I still can't understand how you can talk about alleles so often, and never talk about genes.

If you were saying "how many genes have extant alleles in the popualtion that affect fitness", that I'd understand.  But just wanting a single number of alleles across a population, not caring what genes they belong to?  That's just strange.

If I were to tell you that, across inbred mouse strains, there were 40 alleles that impacted fasting glucose levels, would you really not care to ask how many genes were involved in glucose levels?

 
Quote
If I assume that the average allele is the latter, sometimes beneficial, sometimes harmful, I can simulate this by competing the allele from an element in the first organism, with the allele from the same element in the second, then anti-competing these elements on another occasion.


Okay, what evidence do you have that this is usually the case?  

As opposed to the two alleles being about equally good at whatever it is they do?

 
Quote
The net effect of this, in fact, is that I may as well be taking a random number to represent competing organism 1, and a random number representing competing organism 2, then if either organism has the lucky mutation, incrementing its number by 1, then doing the standard comparison.


So you admit that your simulation doesn't meaningfully take into account what is going on at your 199 other genes.  

What is it that you think you have demonstrated, then?

 
Quote
I know that this is a little strange -- even off beat.


It's not off-beat, its pointless.  You admitted it.  Your sim proves that 1 + a random number > a random number over a lot of trials.  This has nothing to do with evolution.

 
Quote
However, all I am doing in actuality is changing the texture of the noise that the signal is compared to.  With this somewhat unorthodox move, I have removed the problem that the earlier algorithm was having that as other alleles fixed, they reduced the amount of noise I was analyzing.  As such they were dynamically changing the volume of something that I was trying to measure.


But the signal is trivial.  1 + a random number > a random number.  1 > 0.  

 
Quote
As I increase my allele count, evolution continues to happen,


What you are describing is not evolution.

  
bFast



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(Permalink) Posted: Mar. 14 2008,14:39   

Zachriel, we have a problem.

I converted back to my original algorithm for fitness measurement.  In the original algorithm all alleles are equally hurrying towards fixation, however, if I initialize a single organism, the other genes have a huge headstart.  

I made a measurement of the noise I am facing, effectively the integral noise.  The basic premise is that a fixed allele adds no noise to the system, and an evenly split allele adds one unit of noise.  With this algorithm we can see that virtually all of the noise is removed by the time my lucky mutation gets to fixation.  With all of the noise gone, we are not testing the signal to noise ratio any longer.

This result also does not in any way measure the reality of nature.  The allele count of the population remains relatively constant.  The allele count in this version of the sim approaches no polymorphic loci by time it is run.

  
swbarnes2



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(Permalink) Posted: Mar. 14 2008,15:45   

Quote (bFast @ Mar. 14 2008,14:39)
In the original algorithm all alleles are equally hurrying towards fixation, however, if I initialize a single organism, the other genes have a huge headstart.  


Then you should be inducing mutations in the other genes, to give them new alleles.  That's how it happens in real life.

Or weaken the difference between the alleles in the other genes, so that selection isn't as strong in them.

Or institute some kind of non-random mating scheme, so that organisms are more likely to mate with organisms who are more dissimilar.  Sexual selection will partially counter natural selection.

Quote
The allele count in this version of the sim approaches no polymorphic loci by time it is run.


Well yes, selection can get rid of alleles, it can't make new ones.  Darwin figured that out 150 years ago, without a lick of computer time.

  
Reciprocating Bill



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(Permalink) Posted: Mar. 14 2008,17:08   

bfast,

The 1s and 0s employed in your simulation are not at all analogous to alleles, however defined. Because 0s drop out of your total, all your initial assignment of 1s and 0s does is determine how many loci, randomized to either 1 or -1, will contribute to the total. Those values fail to represent alleles of varying adaptiveness because 0s always drop out of the calculation and 1s assume their value randomly at competition time. If any of these values are analogous to alleles, it is 1 versus -1 (addition or subtraction from the total). However, because these signs are not retained beyond a single cycle, calling these "alleles" is simply meaningless. Alleles are passed on, parent to offspring. Your values are discarded.

This procedure also fails to model variable micro-environments that would confer variable adaptiveness to given alleles (which you don't model, in any event). Given that these values are randomized for each cycle, this would be tantamount to every organism awakening daily to an environment that is completely unrelated to the one that obtained the day before, unrelated to the environments to which almost all other organisms are exposed (each of which experiences, in turn a completely unique environment), and to those environments that will arise on the following day.

What does modeling such a circumstance accomplish? There are no ecological contexts that present such variability. Nor would such randomized environments accomplish any selection.

--------------
Myth: Something that never was true, and always will be.

"The truth will set you free. But not until it is finished with you."
- David Foster Wallace

"Here’s a clue. Snarky banalities are not a substitute for saying something intelligent. Write that down."
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Bob O'H



Posts: 2132
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(Permalink) Posted: Mar. 15 2008,03:19   

Quote
Given that these values are randomized for each cycle, this would be tantamount to every organism awakening daily to an environment that is completely unrelated to the one that obtained the day before, unrelated to the environments to which almost all other organisms are exposed (each of which experiences, in turn a completely unique environment), and to those environments that will arise on the following day.

Looks like the conditions for NFL theorems to be applicable.

--------------
It is fun to dip into the various threads to watch cluelessness at work in the hands of the confident exponent. - Soapy Sam (so say we all)

   
Reciprocating Bill



Posts: 4265
Joined: Oct. 2006

(Permalink) Posted: Mar. 15 2008,08:56   

Here is a fragment of bfast's most recent pseudocode:
       
Quote
2: Per cycle, I randomly select two organisms to compete.
- I call a random number < 100,
-   if that number is < "random", I choose the organism that dies by random coin toss.
-   Otherwise I compete them as follows:
-      for element 2 through 10, I call a coin toss.  If heads, I add the fitness of the element for each organism into separate accumulators.  If tails, I subtract the fitness.
-      I add the fitness of element 1 into the accumulator.
-      The organism with the lowest accumulator value is destroyed.
-   I then choose two organisms at random to "mate".  (I could modify my algorithm here to simulate sexual selection.)
-   To mate an organism, I coin toss for each entry in the two organism's arrays, creating a new array.  I then map the strength of each element as described during initialization.
-   I dynamically maintain a count of how many "mutants" are in the array.

bfast -

The bolded statement above is fatal to everything you are attempting to accomplish in your simulation, and prompts the remarks I have made above.  

Your original question was something like, "can natural selection fix an allele in a large population in the presence of considerable noise." But carpet bombing the fitness of each locus of your genome with a random assignment of sign prior to competition, then discarding those signs,  renders all this talk of alleles, fitness, competition, selection, etc. meaningless in the manner I mention above.

That step, introduced to force "the fickleness of natural selection" is a non-sequitur vis the entire preceding discussion and has GOT to GO. It completely and utterly randomizes the fitness contribution of every participating locus of your genome (other than your "lucky" location, which thereby becomes entirely too lucky), and renders meaningless your assertion that 1s and 0s represent alleles.

--------------
Myth: Something that never was true, and always will be.

"The truth will set you free. But not until it is finished with you."
- David Foster Wallace

"Here’s a clue. Snarky banalities are not a substitute for saying something intelligent. Write that down."
- Barry Arrington

  
Wesley R. Elsberry



Posts: 4807
Joined: May 2002

(Permalink) Posted: Mar. 15 2008,10:08   

Back in 1995, I wrote a fairly simple program to simulate random genetic drift in the absence of mutation. The question at issue was whether genetic drift was properly described as heterozygosity loss, as Futuyma and other geneticists had described it. The representation scheme was flexible for number of loci, maximum number of alleles per locus, population size, and number of generations to run. From the messages back then, I was noting that the output pretty well matched a figure in Futuyma's textbook.

I haven't looked at the code in a while, so I don't know offhand how difficult it might be to add mutation and selection to that, or to port it to something other than Pascal. (Though with Free Pascal available for just about any platform, that is not a big issue, either.)

Quote

Simulates genetic drift in a population.  There is complete  replacement at each iteration, panmixia, and independent assortment. The population may be considered to be composed of semelparous sexually reproducing hermaphrodites with possible self-fertilization.


--------------
"You can't teach an old dogma new tricks." - Dorothy Parker

    
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 15 2008,11:16   

Quote (Zachriel @ Mar. 13 2008,18:58)
Quote (bFast @ Mar. 13 2008,17:02)
My current algorithm and reasoning is as follows:

I have no idea what you are doing. What happened to the 2-allele? Are considering only the first gene, which is normally a 0, but once in a population a 1? What's 1/10th the population? I don't get it.

bfast doesn't either.  It is just creationist blathering.

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 15 2008,11:18   

Quote (Zachriel @ Mar. 14 2008,07:07)
You appear to have abandoned your original model because it didn't show what you wanted it to. Perhaps it was trying to tell you something.

Perhaps he is channeling Warren Bergerson?

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 15 2008,12:56   

Allele Blender is beta!



Allele Blender can run a genome size of a few hundred and a population of a few thousand. With sequence length times the size of the population equal to a million, it takes roughly a minute or so per generation.

The current default is just ten genes and a population of 25*25 = 625, starting with a random genome of 0's and 1's. Press ctrl-n to initialize the population. The average fitness should be close to 5 and the standard deviation 1.5, or thereabouts. The other options are set to 10% mutation rate and mating selection for fitness. Mating and colonization are always by proximity.



Now press ctrl-g from any screen to advance a generation. After a few generations (try about ten), these are a few of the characteristics of the population:

  * Average Fitness has increased.
  * Population is highly individualized.
  * Standard deviation is still close to 1.5
  * There are regional differences in population.



Now set the genome size to 100, and generations to 100. Press ctrl-g and take a break. It’ll take a few minutes (about 3 minutes @ 2.5 GHz).  Despite a much larger genome, the results are much the same.


(I’ve limited  the genome size to 1000, but you should be able  to increase this limit up to the integer 32K if you have the available memory. Rows and columns are similarly limited to 100. You can increase these limits in the Declarations module in the VBasic Editor. But I haven’t tested the extreme cases thoroughly.)

3/15 9PM: A few minor updates.
3/16 9AM: Added an option to turn off the display of sequences for very large arrays. Much faster and uses less memory.

--------------
Proudly banned three four five times by Uncommon Descent.
There is only one Tard. The Tard is One.

   
Reciprocating Bill



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(Permalink) Posted: Mar. 16 2008,10:26   

bfast -

I'd be interested in seeing the code for a simulation of intelligent design.

Wouldn't that amount to a hideously long series of assignment statements?

--------------
Myth: Something that never was true, and always will be.

"The truth will set you free. But not until it is finished with you."
- David Foster Wallace

"Here’s a clue. Snarky banalities are not a substitute for saying something intelligent. Write that down."
- Barry Arrington

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 16 2008,11:26   

Quote (Reciprocating Bill @ Mar. 16 2008,10:26)
bfast -

I'd be interested in seeing the code for a simulation of intelligent design.

Wouldn't that amount to a hideously long series of assignment statements?

Isn't tht an interesting proposition - to see IDcreationists actually try to model THEIR OWN ideas to see if they have merit.

nah.

Too risky for them.

  
Reciprocating Bill



Posts: 4265
Joined: Oct. 2006

(Permalink) Posted: Mar. 18 2008,14:00   

Looks like bFast is a one pump chump.

Maybe that explains "bFast."

--------------
Myth: Something that never was true, and always will be.

"The truth will set you free. But not until it is finished with you."
- David Foster Wallace

"Here’s a clue. Snarky banalities are not a substitute for saying something intelligent. Write that down."
- Barry Arrington

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Mar. 19 2008,03:52   

Quote (bFast @ Mar. 12 2008,19:24)
you fear that I have your pet theory by the short hairs.

Then keep pulling bFast! Keep pulling!

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Zachriel



Posts: 2709
Joined: Sep. 2006

(Permalink) Posted: Mar. 24 2008,07:43   

Quote (bFast @ Mar. 14 2008,14:39)
Zachriel, we have a problem.

Well, it's been ten days. And still no answers to my questions. Anyway, here are a few results.

Defaults:

  Generations = 100
  Genes =10
  Genome = Random
  Mutation = 1%
  Mating = Fitness
  Population = 25x25 = 625


Trials (by #genes and mutation rate)

  Genes = 10 (Initial fitness =  ~5)
  Mutation  Fitness (avr., dev.)
  10.0%  54,  2.2
    1.0%  39,  1.4
    0.1%  23,  0.6
 
  Genes = 100 (Initial fitness =  ~50)
  Mutation  Fitness (avr., dev.)
  10.0%  215,  6.5
    1.0%  170,  3.0
    0.1%  123,  1.8
 
  Genes = 1,000 (Initial fitness =  ~500)
  Mutation  Fitness (avr., dev.)
  10.0%   1275,  20.9
    1.0%    931,  11.9
    0.1%    808,    9.4


Trial (by population)

  Genes = 10 (Initial fitness =  ~5)
  Mutation = 1.0%
  Pop  Fitness (avr., dev.)
  10x10   27,  0.8
  25x25   37,  1.4
  100x100  41,  2.0


Now we consider a much larger population, with a very low mutation rate. (With a couple billion gene replications, this took a few hours.)

  Generations = 200
  Genes = 1000 (Initial fitness =  ~500)
  Mutation = 0.01%
  Mating = Fitness
  Pop =100x100 = 10,000




Fitness began at ~500 and has increased to ~2158. With a thousand genes and several alleles (~7) for each gene, we have a very diverse population — despite the very low mutation rate. Due to recombination, even close relatives are unique individuals.

With such large sequences, it can be difficult to visually determine family relationships, but a look at Beauty (not under selection) reveals interesting regional patterns.



So we can see many of the aspects we expect from an evolutionary process. Individualism, descendant families, regional variations, a variety of alleles for each gene persisting in the population, increasing average fitness (even if, as in other examples, mating selects for a non-fit trait, the peacock's tail), weighted distributions of sequence fitness and allele distribution, etc.

All we did was add a dash of random mutation to bFast's original concept.

--------------
Proudly banned three four five times by Uncommon Descent.
There is only one Tard. The Tard is One.

   
dogdidit



Posts: 315
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(Permalink) Posted: Mar. 24 2008,09:31   

Quote (Zachriel @ Mar. 24 2008,07:43)
       
Quote (bFast @ Mar. 14 2008,14:39)
Zachriel, we have a problem.

Well, it's been ten days. And still no answers to my questions.

Nor are any answers expected. bFast was working backwards from his conclusions, which were the same as his assumptions.

But thanks anyway, Zachriel, for completing Allele Blender. I have an idle interest in evolutionary computation, but it never occured to me that Excel could be used so ably as a tool for prototyping and visualization. Nice work! Now if I only knew squat-all about VBA...

To the other forum members:
I feel I should apologize for not using my name as my username when I came aboard. This is the first internet forum I have participated in, and anonymity seemed prudent when I registered. "dogdidit" is an obvious play on "goddidit", but my wife and I also raise shelties so "dog did it" is a frequent explanation for an endless sequence of household misadventures. I'm even contemplating a canine LOLcat for an avatar. Uh, LOL.

I had intended to stay as a mere guest here (this is a fun place to kibbitz) but when I saw bFast use the term "signal to noise", my thirty plus years of experience in radar and communications engineering told me to sit up and pay closer attention. Hey, that's MY stuff! I've grown weary from engineers' frequent resort to (bad) reasoning by analogy - the brain as a computer, DNA as software - and I was suspicious that this was another example of a misleading metaphor. Or is this a term commonly encoutered in genetics or molecular biology?

Well, I won't overstay my welcome. Cheers!

Tom Moloney-Harmon
BS Physics, Harvey Mudd College
MSEE, Johns Hopkins University
Science nerd

<And now, ladies and gentlemen, back to your internet forum discussions, which are already in progress...>

--------------
"Humans carry plants and animals all over the globe, thus introducing them to places they could never have reached on their own. That certainly increases biodiversity." - D'OL

  
Freelurker



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(Permalink) Posted: Mar. 24 2008,14:01   

Quote (dogdidit @ Mar. 24 2008,10:31)
 
I feel I should apologize for not using my name as my username when I came aboard.

No need to apologize; many of us here choose to remain anonymous.
     
Quote

... my thirty plus years of experience in radar and communications engineering told me to sit up and pay closer attention. Hey, that's MY stuff!

Greetings from a fellow engineer. There are a few of us who comment here and who are critical of ID.
     
Quote
I've grown weary from engineers' frequent resort to (bad) reasoning by analogy - the brain as a computer, DNA as software -

Please be careful with that broad brush! That behavior is typical of ID/Creationist engineers; analogies are all they have. Also watch for their continual equivocation on the word "design."
     
Quote
and I was suspicious that this was another example of a misleading metaphor. Or is this a term commonly encoutered in genetics or molecular biology?

I've been wondering about that too. The biologists here were more tolerant of the signal-and-noise analogy than I expected.

As to bFast, we are talking about a guy who agrees with a statement that engineering can be methodologically non-materialistic. Too bad the moderator at UD didn't let me follow up on that one.
See:
http://tinyurl.com/32nsh6

And now bFast has gone back to the cloister.

BTW, hats off to Zachriel, who set the best example of how bFast's comments should be handled. And a slight hat tip to bFast himself, who at least tried to do some modelling, not just philosophizing.

Edit: 1)fixed link, 2)more than a few

--------------
Invoking intelligent design in science is like invoking gremlins in engineering. [after Mark Isaak.]
All models are wrong, some models are useful. - George E. P. Box

  
slpage



Posts: 349
Joined: June 2004

(Permalink) Posted: Mar. 24 2008,17:46   

That is his way.  He did the same thing at evolutionisdead.com when his claims were questioned - spewed a few insults then runs back to tard-protection land.

IDiots are intellectual cowards.  Or should I say pseudointellectual cowards - even extreme mesomorph and failed jarhead Davey Springer.

  
Reciprocating Bill



Posts: 4265
Joined: Oct. 2006

(Permalink) Posted: Mar. 24 2008,18:38   

Quote (dogdidit @ Mar. 24 2008,10:31)
I feel I should apologize for not using my name as my username when I came aboard.

You damn well better. On the day I was born my mama looked me in the eye and said, "I'm gonna name you Reciprocating." And here I am Mama! Here I am, it's your boy Reciprocating! Ain't you proud of me Mama? Mama?

But now that you have uncloaked, sit down a spell.

--------------
Myth: Something that never was true, and always will be.

"The truth will set you free. But not until it is finished with you."
- David Foster Wallace

"Here’s a clue. Snarky banalities are not a substitute for saying something intelligent. Write that down."
- Barry Arrington

  
Richardthughes



Posts: 10756
Joined: Jan. 2006

(Permalink) Posted: Mar. 24 2008,21:01   

Quote (slpage @ Mar. 24 2008,17:46)
IDiots are intellectual cowards.  Or should I say pseudointellectual cowards - even extreme mesomorph and failed jarhead Davey Springer.

I has scarded him offs a few times.

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"Richardthughes, you magnificent bastard, I stand in awe of you..." : Arden Chatfield
"You magnificent bastard! " : Louis
"ATBC poster child", "I have to agree with Rich.." : DaveTard
"I bow to your superior skills" : deadman_932
"...it was Richardthughes making me lie in bed.." : Kristine

  
Cedric Katesby



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Joined: Aug. 2006

(Permalink) Posted: Mar. 25 2008,10:46   

"BTW, hats off to Zachriel, who set the best example of how bFast's comments should be handled. And a slight hat tip to bFast himself, who at least tried to do some modelling, not just philosophizing."

Hear, hear!

  
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