Annoying creationists

[delphi_ote]

Anyone interested in HIV evolution should check out the March 16th issue of Science. There's a fantastic publication on recent discoveries using phylogenetic analysis concluding that, "Virus variability may not be as predictable as first thought, making it harder to cover the variation of HIV by vaccines."

Taffer, you'd probably really dig it, what with your being a phylogeneticist and all. The idea that the virus has a phylogeny within a host and between hosts is definitely interesting. If you have experience with that type of thing, I'd love to hear about it!

The Science publication makes this whole discussion about multiple selection pressures seem silly. In the summary of this cutting edge research by the greatest minds of our day on the very topic we're discussing, we read that, "the extraordinary power of viruses like HIV and HCV to escape almost any means of host attack remains a daunting hurdle to overcome."

 

[Taffer]

Anyone interested in HIV evolution should check out the March 16th issue of Science. There's a fantastic publication on recent discoveries using phylogenetic analysis concluding that, "Virus variability may not be as predictable as first thought, making it harder to cover the variation of HIV by vaccines."

Taffer, you'd probably really dig it, what with your being a phylogeneticist and all. The idea that the virus has a phylogeny within a host and between hosts is definitely interesting. If you have experience with that type of thing, I'd love to hear about it!

The Science publication makes this whole discussion about multiple selection pressures seem silly. In the summary of this cutting edge research by the greatest minds of our day on the very topic we're discussing, we read that, "the extraordinary power of viruses like HIV and HCV to escape almost any means of host attack remains a daunting hurdle to overcome."

I had a quick look at it online, and it looks really interesting! Tomorrow I will go to the uni and see if I can nab a copy to read over. Thanks for pointing it out to me.

Oh, and FWIW, I'm not a phylogeneticist yet, only a grad student in genetics. But I have specialized into phylogenetics and evolution, and my research project is a phylogenetics one (we are doing the phylogenetics of a certain family of native New Zealand snails at the genra level, and also interspecifically, using several genes).

 

[Taffer]

Apology

No, I am not. Given that I am, in essence, a population geneticist (ok, a phylogeneticist, but same difference ), I trust my own studies over what you say. Secondly, evolution is defined as the change in alleles over time. There is no difference between "recombination and natural selection" from "mutation and natural selection". Natural selection works on any existing variation in a population, no matter how that variation arose.

I take back the bolded section. I am a phylogenetics grad student, not an actual phylogeneticist. However, over the course of my studies, I have delt with a lot of population genetics (and phylogenetics, obviously), and so, while I do not claim to be an expert by any stretch of the imagination, at least I am familiar with the subject material. I apologize to anyone who got the impression that I am a practicing phylogeneticist.

 

[The Great Hairy One]

I've forgotten most of the population genetics I did at uni. Sooo long ago. I do remember calculating allele frequencies in populations, and all that stuff. Anyway, I preferred the more lab orientated stuff. Breeding Drosophila and stuff.

Cheers,
TGHO

 

[Paul C. Anagnostopoulos]

Try 1 mutation per 100 bases in your series and I think you will see the paraboloid behavior of the curve.

Oh yes, I see. You're cranking the rate up so high that you're introducing some sort of mutational overload. I think I saw that when I increased the rate above 1 mutation per 180 bases or so.

However, I'm talking about 4 mutations per genome vs. your 1 mutation per genome. I don't think the overload comes into consideration then. How many generations did you run that experiment before you concluded that evolution had stopped?

Evolutionists have mistakenly extrapolated microevolutionary processes to macroevolution. There are no selection processes to do this.

This claim is meaningless until you define macroevolution.

~~ Paul

 

[Mr. Scott]

Annoying Cats

This [Kleinman's] claim is meaningless until you define macroevolution.

I'd been thinking about this and want to provide an example as food for thought for Dr. Kleinman.

I once read that it was discovered that the cat family branched from its ancestors (more dog-like IIRC) when the gene that allowed them to taste sweetness was damaged (I guess by a point mutation). Scientists found a gene necessary for the sensing of sugars to be complete in the cat family except for a mutation that completely crippled it. The parent mammals had a sweet tooth and were omniverous. The child had no sweet tooth and was completely disinterested in eating anything but meat -- almost purely carniverous.

Here we had a point mutation microevolutionary step that profoundly affected the lifestyle of the animal -- the kind of step Dr. Kleinman asserts gives no problem to the Ev program or to a literal interpretation of Bible.

Now, if we have an omnivore that's lost its taste for everything but meat, we have a creature that better become a good predator, and better get most of its dietary needs from it. While not a fatal mutation at first, it obviously engaged selective pressures towards prefecting its predatory skills.

In each microevolutionary step, a random mutation could have modified our proto-cat's ability to hunt. A microevolution to the ear shape so it could hear its prey better, to its eye shape to see, its binocular vision to lock on to a target, its paw shape to walk more stealthily, and so on, and so forth. Many, many microevolutionary steps later, and we have a mammal that appears to bronze age men to be not at all related to similar predators, and it accumulated too many microevolutionary changes to mate with it's distant cousins (I presume -- has anyone tried to make a cog or a dat?). The cat, because of its perfection as a meat eater without backup of eating plants, became that most perfect predator on land. It's easy to understand intuitively how this run of micro-evolutionary changes, each of which Dr. Kleinman couldn't dispute as "mathematically impossible," would add up to a macroevolutionary transformation after millions of years.

OK, Dr. Kleinman, prove mathematically that dogs and cats could not have diverged from a common ancestor. Apparently, there is evidence that they did. I don't think extrapolating from the HIV antiviral drug treatments or a partial computer simulation of evolution could do this. You'll need more than that.

 

[kleinman]

Annoying Creationists

No macroevolution has ever taken place in the real world.

Macroevolution is not a meaningful distinction in evolutionary theory.

That’s obvious.

No macroevolution has ever occurred, that is what your computer model shows and that is what triple antiviral medications for the treatment of HIV shows. Care to describe the selection process that evolved the original HIV virus. If you say simian virus, I’ll ask how the simian virus evolved.

Triple antiretrovirals have nothing to do with 'macroevolution', nor do they have anything to do with the subject at hand. They are used because three antiretrovirals kill faster then one. They also decrease the risk of any one resistance evolving at a particular time, but it does not decrease the probability of triple resistance mutants arising

First of all, there are no antiretrovirals that kill the virus. Antiretrovirals impair a particular metabolic step whether it be in reproduction of the virus or some other step in the life cycle of the virus. Once you have HIV, you always have HIV. Second, the mutations seen which lead to drug resistance in HIV change the molecular structure of the particular enzyme sufficiently that the drug can no longer act effectively. There are no new enzymes being produced. Third, I have no idea how you compute the probability that resistance will occur one drug at a time vs resistance to three drugs simultaneously.

That is correct Taffer, so what is the selective pressure that evolved the original HIV?

I believe there is lots of evidence for the evolution of the HIV virus. See

here for a very brief run down on the origins of HIV.

So, how did the simian virus evolve?

So you think that three new mutant alleles can evolve simultaneously as quickly as three new mutant alleles evolving one after another?

Yes, of course. The chance of a mutant allele arrising at any one loci is fixed and independant on the number of other mutations arrising on the genome.

Too bad the mathematics of ev doesn’t show this and why are the infectious disease experts subjecting people with HIV to all the adverse drug reactions of multiple drug therapy?

Taffer, you are confusing recombination and natural selection with mutation and natural selection.

No, I am not. Given that I am, in essence, a population geneticist (ok, a phylogeneticist, but same difference ), I trust my own studies over what you say. Secondly, evolution is defined as the change in alleles over time. There is no difference between "recombination and natural selection" from "mutation and natural selection". Natural selection works on any existing variation in a population, no matter how that variation arose.

Ok expert in phylogenetics, how did the first allele arise?

The mutations that occur with HIV are usually single base substitutions. In order to achieve resistance to three antiviral agents simultaneously, you must have all three random mutations appear simultaneously. If a particular virus manages to become resistant to one agent, it still must content with the selective pressure of the other two agents which is slowing down the reproduction of this strain resistant to the one drug. The net result either way is that multiple selective pressures slow down the evolutionary process.

No it isn't, and you obviously do not understand how antivirals work. Most, if not all, antivirals do not lead to a complete death of the virus. The slow the rate of viral infection, but not 100% of viruses are killed. Thus, a virus which evolves resistance to a single antiretroviral agent will have an advantage over its peers, as it is only being selected for by two selection pressures, not three. Stop thinking in black-and-whites. Biology does not work that way.

Triple antiretrovirals have nothing to do with 'macroevolution', nor do they have anything to do with the subject at hand. They are used because three antiretrovirals kill faster then one. They also decrease the risk of any one resistance evolving at a particular time, but it does not decrease the probability of triple resistance mutants arising

I added the color. Could you get your story straight.

Dr Schneider’s 3 dimensional fitness landscape already shows bad news for the theory of evolution. I suggested to Paul to modify ev to evolve two sets of binding sites with 6 selection conditions. I doubt he will do this because it is now quite apparent what ev does with 3 selection conditions. He knows I will co-opt this work.

Whatever, kleinman. Since you have shown to have little to know understanding of even basic microbiology, evolutionary theory or population theory, I will trust population and evolutionary genetics over what you claim anyday. Since I have done the maths myself, I know 3 dimensional fitness landscapes work.

Really, do you know how fitness landscapes work as well as how antiretrovirals work? In one sentence you say they kill the virus and the next you say they don’t.

Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.

So Delphi, why don’t you give us a quote from your Science publication that shows that multiple selection pressures for treating the virus seem silly?

No, I am not. Given that I am, in essence, a population geneticist (ok, a phylogeneticist, but same difference ), I trust my own studies over what you say. Secondly, evolution is defined as the change in alleles over time. There is no difference between "recombination and natural selection" from "mutation and natural selection". Natural selection works on any existing variation in a population, no matter how that variation arose.

I take back the bolded section. I am a phylogenetics grad student, not an actual phylogeneticist. However, over the course of my studies, I have delt with a lot of population genetics (and phylogenetics, obviously), and so, while I do not claim to be an expert by any stretch of the imagination, at least I am familiar with the subject material. I apologize to anyone who got the impression that I am a practicing phylogeneticist.

Apology accepted.

Try 1 mutation per 100 bases in your series and I think you will see the paraboloid behavior of the curve.

Oh yes, I see. You're cranking the rate up so high that you're introducing some sort of mutational overload. I think I saw that when I increased the rate above 1 mutation per 180 bases or so.

What is your problem? If you want to study the parametric behavior of ev, you go through the range of values and see what kind of curve is obtained. You don’t think a mutation rate of 1 mutation per 256 bases per generation will give mutational overload to any real living thing?

However, I'm talking about 4 mutations per genome vs. your 1 mutation per genome. I don't think the overload comes into consideration then. How many generations did you run that experiment before you concluded that evolution had stopped?

I’m no longer sure which experiment you are talking about. Choose a series you want to look at, (genome length, mutation rate, etc.) and we will show everyone when ev converges and when ev stops converging. Then I will show you on the case where ev does not converge, eliminating any two of the three selection conditions will allow ev to evolve that particular condition. It is the multiple conflicting selection conditions that stops ev from converging.

Evolutionists have mistakenly extrapolated microevolutionary processes to macroevolution. There are no selection processes to do this.

This claim is meaningless until you define macroevolution.

Paul, I’ve defined it by example. I’ll repeat some of the examples here. The evolution of a gene from the beginning, the transformation of a gene from some original function to some totally new function and the evolution of humans and chimpanzees from a primate ancestor. Here are some examples of microevolution. The evolution of drug resistant strains of HIV, Sickle cell hemoglobin and recombination events are all examples of microevolution.

This [Kleinman's] claim is meaningless until you define macroevolution.

OK, Dr. Kleinman, prove mathematically that dogs and cats could not have diverged from a common ancestor. Apparently, there is evidence that they did. I don't think extrapolating from the HIV antiviral drug treatments or a partial computer simulation of evolution could do this. You'll need more than that.

Mr Scott, I’ve already proved mathematically that ev can’t evolve binding sites on a realistic length genome because of the multiple selection conditions. If you can’t evolve simple binding sites, what makes you think you can evolve the huge number of genetic differences between cats and dog from a common ancestor? Do you want to tell us what the selection conditions that do this? Paul can then put it in ev and end this discussion.

By the way, do you consider a picture of a dog and cat with similar markings as your evidence that they evolved from a common ancestor? That is a cute picture though.

 

[delphi_ote]

So Delphi, why don’t you give us a quote from your Science publication that shows that multiple selection pressures for treating the virus seem silly?

You've changed your claim from "slowing/stopping evolution" to "treating the virus." Any particular reason for that?

Also, it's not my Science publication.

 

[kleinman]

Annoying Creationists

So Delphi, why don’t you give us a quote from your Science publication that shows that multiple selection pressures for treating the virus seem silly?

You've changed your claim from "slowing/stopping evolution" to "treating the virus." Any particular reason for that?

You evolutionists have such weak arguments that you have to parse words to try to find anything to argue. HIV is treated by using multiple selection pressures. These multiple selection pressures slow the evolution of drug resistant strains because it either requires that multiple beneficial mutations occur simultaneously or if a single beneficial mutation occurs, the other drugs suppress the reproduction of the virus, either way it slows evolution. There is a distinction between treating and curing a disease.

Also, it's not my Science publication.

That’s right, your niche is gene duplication but you still won’t tell us how the original gene appeared.

You appeared to start to understand why multiple selection pressures slow evolution. This is the very heart of the theory of evolution. Ev shows mathematically why multiple selection pressures slow this process. It is now obvious that when you have multiple selection conditions, the only way you can advance all the selection conditions simultaneously is that a given creature have nothing but beneficial mutations. Otherwise, combinations of good and bad mutations confound the evolutionary process. How do you evolve all the genes that code for the enzymes of the Krebs cycle? Even more incomprehensible is how do you evolve all the genes required for the DNA replicase system, especially since without these enzymes you can’t replicate DNA? What are the selection processes that would accomplish such events? How can these events occur serially when parallel selection conditions (if you could describe them) slow if not completely stop the evolutionary process. Mutation and selection is a much more limited phenomena than you evolutionist like to make it. The mathematics shown by ev reveals this and there are real examples of this.

 

[Paul C. Anagnostopoulos]

What is your problem? If you want to study the parametric behavior of ev, you go through the range of values and see what kind of curve is obtained. You don’t think a mutation rate of 1 mutation per 256 bases per generation will give mutational overload to any real living thing?

I have no idea, but we are talking about the way Ev behaves, not the way the real world behaves. At some point, mutation overload occurs. Meanwhile, generations appears to be linear with mutation rate until that point.

Alan, not only are you claiming that evolution in Ev stops dead, but then you are extrapolating this to the real world.

I’m no longer sure which experiment you are talking about. Choose a series you want to look at, (genome length, mutation rate, etc.) and we will show everyone when ev converges and when ev stops converging. Then I will show you on the case where ev does not converge, eliminating any two of the three selection conditions will allow ev to evolve that particular condition. It is the multiple conflicting selection conditions that stops ev from converging.

I'm talking about these parameters:

population 64
genome size 16,384
binding sites 16
weight/site widths 5/6
1 mutation per generation

How long did you run that before you concluded that it had stopped evolving?

You appeared to start to understand why multiple selection pressures slow evolution. This is the very heart of the theory of evolution. Ev shows mathematically why multiple selection pressures slow this process.

Wait, a bit ago you were claiming that multiple pressures stop the process.

~~ Paul

 

[Dr Adequate]

Lie #1.

Truth #1.

Come back when you have some new lies, you boring whining little freak.

 

[Dr Richard]

This claim is meaningless until you define macroevolution.

Good luck Paul! I suspect that this question is futile until you define goalposts

If you ever get an answer, could you then ask Kleinman whether a 491 base-pair difference between genes is a "micro-" or "macro-" evolutionary event?

http://www.genetics.org/cgi/content/abstract/175/3/1071

(In fruit flies, a wandering "selfish" gene inserted itself upstream of a gene that is able to confer resistance to insecticides such as DDT, and left behind some of itself. The residual DNA (a 491 base pair long terminal repeat) doubles the expression of said gene in tissues useful for breaking down ingested toxins (such as the gut), and perhaps not suprisingly is now the dominant allele).

 

[kleinman]

Annoying Creationists

What is your problem? If you want to study the parametric behavior of ev, you go through the range of values and see what kind of curve is obtained. You don’t think a mutation rate of 1 mutation per 256 bases per generation will give mutational overload to any real living thing?

I have no idea, but we are talking about the way Ev behaves, not the way the real world behaves. At some point, mutation overload occurs. Meanwhile, generations appears to be linear with mutation rate until that point.

Well Paul, your retreat from your previous statement is complete. Recall when you said this on http://www.internationalskeptics.com/forums/showthread.php?t=48008&page=6 ?

There are plenty of examples of A-life evolving. I think Ev rankles the IDers because it is a model of actual life, and also because Schneider is fairly good at advertising it.

So how many years have you spent modeling unreality? By the way, I consider myself a creationist, maybe that is why ev doesn’t rankle me. In fact, I really enjoy this model. Do you have any other models you are planning to do, I really like your work. Talk about moving goalposts. I think you just entered one of kjkent1’s alternative universes.

You can put linear curve fits to a portion of the mutation/generation for convergence curve.

Alan, not only are you claiming that evolution in Ev stops dead, but then you are extrapolating this to the real world.

The example of the evolution of HIV drug resistance is not extrapolation. You know that ev stops dead when you reach what you call the Rcapacity value. It is very easy to show that if you remove two of the three selection conditions that the third condition will evolve despite exceeding your Rcapacity value.

I’m no longer sure which experiment you are talking about. Choose a series you want to look at, (genome length, mutation rate, etc.) and we will show everyone when ev converges and when ev stops converging. Then I will show you on the case where ev does not converge, eliminating any two of the three selection conditions will allow ev to evolve that particular condition. It is the multiple conflicting selection conditions that stops ev from converging.

I'm talking about these parameters:

population 64
genome size 16,384
binding sites 16
weight/site widths 5/6
1 mutation per generation

How long did you run that before you concluded that it had stopped evolving?

I stopped this case at 400,000 generations because no selection was occurring. Feel free to run this case for a longer period. I notice your case with 4 mutations/G has run 800,000 generations and appears to be converging which is ok with me because even with only 1 mutation/G, this case will evolve individual selection conditions in:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
When you get your case to converge, you can do the G=64k, 128k, 256k… with three selection conditions and I’ll show how quickly the individual selection conditions converge for the cases.

When you get finished with those cases, would you do a version of ev that evolves two sets of binding sites simultaneously? Let’s see if six selection conditions can evolve simultaneously on a 256 base genome.

You appeared to start to understand why multiple selection pressures slow evolution. This is the very heart of the theory of evolution. Ev shows mathematically why multiple selection pressures slow this process.

Wait, a bit ago you were claiming that multiple pressures stop the process.

The HIV case shows the slowing of evolution with multiple selection pressures. Ev shows both the slowing and ultimately the stopping of evolution with multiple selection pressures. When you do the two sets of binding sites version of ev, you can show how much more quickly evolution stops with 6 selection conditions.

This claim is meaningless until you define macroevolution.

Good luck Paul! I suspect that this question is futile until you define goalposts

If you ever get an answer, could you then ask Kleinman whether a 491 base-pair difference between genes is a "micro-" or "macro-" evolutionary event?

There you go Paul, put transposons in your model and that solves your mathematical conundrum. Hey Dr Richard, when are you going to tell us how the ancestral insulin gene evolved from the beginning? Paul, maybe you should ask Dr Richard this question, it appears he is not talking with me any more. Dr Richard, I don’t care if you dropped out of Sesame Street, I’ll still talk with you.

Goalposts? Paul originally said ev models actual life, but now he says ev does not behave the way the real world behaves. Well, I told Dr Schneider that once people understood his model, they would discredit the model. Now his own programmer is doing this. Dr Schneider, I am still with you and your model.

 

[kjkent1]

Dr Schneider, I am still with you and your model.

LOL! This is a riot. You contradict yourself in just about every other post.

I'm still trying to avoid sitting down at Dr. Adequate's table, but the only other seat available appears to be one with a view of you sitting on a bus bench wearing an aluminum hat!

I will give you this: you've managed to convince just about everyone here that ev works pretty much as advertised.

When will we see your paper rebutting ev? Certainly the Discovery Institute would pay you big bucks to publish your findings.

 

[kleinman]

Annoying Creationists

Dr Schneider, I am still with you and your model.

LOL! This is a riot. You contradict yourself in just about every other post.

You got this confused. It is ev that contradicts the theory of evolution. Why do you think that Paul now says ev does not behave the way the real world behaves. Perhaps he is in one of you 10^500 alternative universes.

I will give you this: you've managed to convince just about everyone here that ev works pretty much as advertised.

You did read the fine print in the advertisement?

When will we see your paper rebutting ev? Certainly the Discovery Institute would pay you big bucks to publish your findings.

When will we see you present a marketing plan to your company so we can do cases with realistic genome lengths and large populations. We still haven’t completely driven that nail in the theory of evolution coffin.

 

[kjkent1]

When will we see you present a marketing plan to your company so we can do cases with realistic genome lengths and large populations. We still haven’t completely driven that nail in the theory of evolution coffin.

Write a research proposal detailing your hypothesis and experiment, the resources you believe will be necessary to prove your experiment, and the rationale for why the experiment is important to the general scientific community.

Both you and Dr. Schneider must agree, in writing, that the experiment, as proposed will resolve a fundamental scientific question concerning evolutionary biology, and that you each reasonably believe that this experiment is important enough to command the attention of major scientific publications (Nature, Science, etc.).

Alternatively, you may construct and wear an aluminum hat.

 

[Paul C. Anagnostopoulos]

I stopped this case at 400,000 generations because no selection was occurring. Feel free to run this case for a longer period. I notice your case with 4 mutations/G has run 800,000 generations and appears to be converging ...

I think you missed the big news in post #3306:

After 1,083,137 generations, a creature with zero mistakes has emerged from the primordial depths. It has an Rsequence of 11.13, higher than the Rfrequency of 10 and lower than the Rcapacity of 12. The sequence logo is ACGACA.

So you were running an experiment that should take at least four times as long, and you quit at 400,000 generations?! From this you concluded that evolution can stop.

Ev shows both the slowing and ultimately the stopping of evolution with multiple selection pressures. [emphasis mine]

Not according to that experiment, it doesn't.

~~ Paul

 

[kleinman]

Annoying Creationists

I stopped this case at 400,000 generations because no selection was occurring. Feel free to run this case for a longer period. I notice your case with 4 mutations/G has run 800,000 generations and appears to be converging ...

I think you missed the big news in post #3306:

Well, let’s repeat that post here:

I am running the following experiment:

population 64
genome size 16,384
binding sites 16
weight/site widths 5/6
4 mutations per generation

These are identical to your parameters, except for 4 mutations per generation instead of 1. This should make no difference, since your argument has nothing to do with mutation rate. After 800,000 generations the mistake count is 4. It hasn't "stopped" yet. I'll let you know if it does.

Well, it doesn't. After 1,083,137 generations, a creature with zero mistakes has emerged from the primordial depths. It has an Rsequence of 11.13, higher than the Rfrequency of 10 and lower than the Rcapacity of 12. The sequence logo is ACGACA.

So with a mutation 4 times higher than I used, you can get all three selection condition to converge in a little more than a million generations. For the same length genome and a mutation rate of 1 per genome per generation you get the following:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
So far, evolution hasn’t stopped for three selection conditions on a 16,384 base genome but I think you can say that it has slowed down a bit since each individual selection condition converges more than a thousand times faster.

After 1,083,137 generations, a creature with zero mistakes has emerged from the primordial depths. It has an Rsequence of 11.13, higher than the Rfrequency of 10 and lower than the Rcapacity of 12. The sequence logo is ACGACA.

Were having so much fun with this, let’s do the 32k, 64k, 128k and 256k genomes. My data is for 1 mutation per 256 bases per generation for all these cases. Other parameters are the same as your case except where noted.
G /Gens PC/bind/spur gen/spur out gen
65536 /1/ 1/ 0/ 0
65536 /5/ 0/ 1/ 0
65536 /18/ 0/ 0/ 1
131072/1/ 1/ 0/ 0
131072/17/ 0/ 1/ 0
131072/27/ 0/ 0/ 1
262144/3/ 1/ 0/ 0/ pop 32
262144/1/ 0/ 1/ 0
262144/15/ 0/ 0/ 1
In order to run the 256k case, I had to reduce population to 32. I’ll let you run these cases with all three selection processes operating and you can refute my argument the evolution doesn’t stop.

So you were running an experiment that should take at least four times as long, and you quit at 400,000 generations?! From this you concluded that evolution can stop.

I’ll remember this, I won’t give up so easily next time.

Ev shows both the slowing and ultimately the stopping of evolution with multiple selection pressures. [emphasis mine]

Not according to that experiment, it doesn't.

Now don’t you give up so easily, you have the 32k case to run. Isn’t that one where Rcapacity=Rfrequency? Then when you finish that one, you have the 64k, 128k and 256k genomes to do. So enjoy your fleeting victory because I’ve already shown that these other cases easily converge when using only a single selection condition.

Just a question to finish this post. If the number of generations required to converge your cases exceeds the time available in the age of the universe, does that qualify as evolution stopping? That’s ok with me, so you can stop your cases when they exceed:

(4 billion years)*(365days/year)*(1 generation/day) = 1,460,000,000,000 generations.

If you want to use the reproductive rate for bacteria, feel free to run you simulation a little longer.

This is fun!

 

[kjkent1]

Well, let’s repeat that post here:

So with a mutation 4 times higher than I used, you can get all three selection condition to converge in a little more than a million generations. For the same length genome and a mutation rate of 1 per genome per generation you get the following:
missed site/spurious binding-gene/spurious binding outside gene/gens to perfect creature
1/0/0/7
0/1/0/223
0/0/1/233
So far, evolution hasn’t stopped for three selection conditions on a 16,384 base genome but I think you can say that it has slowed down a bit since each individual selection condition converges more than a thousand times faster.

Were having so much fun with this, let’s do the 32k, 64k, 128k and 256k genomes. My data is for 1 mutation per 256 bases per generation for all these cases. Other parameters are the same as your case except where noted.
G /Gens PC/bind/spur gen/spur out gen
65536 /1/ 1/ 0/ 0
65536 /5/ 0/ 1/ 0
65536 /18/ 0/ 0/ 1
131072/1/ 1/ 0/ 0
131072/17/ 0/ 1/ 0
131072/27/ 0/ 0/ 1
262144/3/ 1/ 0/ 0/ pop 32
262144/1/ 0/ 1/ 0
262144/15/ 0/ 0/ 1
In order to run the 256k case, I had to reduce population to 32. I’ll let you run these cases with all three selection processes operating and you can refute my argument the evolution doesn’t stop.

This is fun!

Yes it is fun. Observe exactly how fun this is, Alan.

The first creature appeared in the first generation, because it was first. Therefore, no selective pressures could have existed.

Your experiments confirm that the first creature could have easily appeared instantly from the primordial soup, regardless of the length of its genome, because low and behold, it routinely appears in the first generation of your ev experiments.

Congratulations Alan! You've demonstrated abiogenesis via ev.

You may now collect your Nobel Prize. Alternatively, you may construct and wear an aluminum hat.

 

[kleinman]

Annoying Creationists

This is fun!

Yes it is fun. Observe exactly how fun this is, Alan.

The first creature appeared in the first generation, because it was first. Therefore, no selective pressures could have existed.

Is that what you think this data says? What is says it is very easy for sequences of bases to satisfy the threshold for the weight matrix. It is so easy that there were no mistakes in identifying binding sites. The weight matrix is able to recognizes binding sites starting with a random genome. Now getting rid of the many spurious binding sites takes a few generations but it doesn’t take long. If you want to learn something about the behavior of ev, run these cases in the step mode and watch what happens to the mistake counts. I don’t suggest using the step method when doing cases with three selection conditions. You will get a repetitive use injury of your index finger long before these cases converge (if they ever will converge).

Now there is another explanation, your string cheese theory of evolution and we are running these cases in one of your 10^500 alternative universes.