Annoying creationists

[rocketdodger]

Which is odd. When you wipe out 90% of a population and the rest has adapted to said pressure, then evolution has proceeded much more rapidly.

Well, the argument that Adequate and I are using only works if you have both a sufficient number of pressures and sufficient time for all of their targeted mutations to fixate. If the pressures are extremely lethal, the combination of them will kill off the population before any of that happens.

Which kind of begs the question why Kleinman uses this scenario in the first place -- of course there will be no evolution, the population is dead.

 

[kleinman]

Annoying Creationists

Rocketdodger, you are wrong about this, there is one thing more that you have to add to your description. How does this mutation and selection process work mathematically and empirically?

Did you even read my post? Obviously not, because I made it very clear exactly how mutation and selection works mathematically -- mutations affect the chances their carriers have of passing them on to the next generation. It is that simple Kleinman.

No you haven’t shown how mutation and selection works mathematical, you posted a hunch. Dr Schneider’s model shows mathematically how mutation and selection works and I have posted hundreds of citations which show how mutation and selection works empirically. Dr Schneider’s model and these citations show that combination selection pressures profoundly slow the mutation/selection, sort/optimization process. Your hunch shows noting about how mutation and selection actually works.

Again rocketdodger, you are wrong about this, the environment does the sort.

No. The environment is an inanimate object. How you think it could possibly sort anything is beyond me.

So are you claim that sorting is done only by animate objects? Who was the animator in the primordial soup?

The individuals who have the best fitness in given environment are able to reproduce; this is not determined by the individuals themselves.

So you contend that a race track sorts the field, rather than the drivers? The environment determines which individuals have the most relative fitness, but the individuals themselves do the reproducing or the dying.

Sure the track affects the race. If you have water on the track, cars with tires suitable for wet surfaces perform better than those that do not. If the track dries out, tires suitable for dry surfaces give better performance. If the population does not have the resources to reproduce in a given environment, it is not up to the population whether it lives to reproduce or die. These matters are out of the hands of the population.

Rocketdodger, mutation and selection is not somewhat analogous to sorting, it is exactly analogous.

Except for the two differences I pointed out, of course. Selection happens in O(1) time. Sorting can't happen faster than O(nlogn) time.

You have introduced O(bscure) terminology. Mutation and selection is nothing more than a sorting/optimization problem but don’t let me stop you from trying to prove that n+1 selection pressures evolve more rapidly than n selection pressures. While you are at it, why don’t your write server software that performs faster as more users access the server.

And the rate can be measured by the number of generations required to evolve a given number of loci for a given size genome, population, mutation rate and number of selection conditions. If read the earlier portions of this thread, you will see that was what was done with ev.

Yes. The important point is that the average rate is more important than the instantaneous rate, which you seem to agree with.

Yes, I would tend to agree with that when you are talking about stochastic processes. Often time evolutionists try to argue that a single big change can explain what is measured. The problem for evolutionists is that when there large genetic changes, they are catastrophic for the individual who has this large genetic mutation.

You are missing an important point. The way selection pressures affect the population is by changing the frequency of particular sequences of bases. That’s how a population finds a trajectory on the fitness landscape to a new local optimum.

The notion of a "fitness landscape" and "local optimum" are non-existent in reality. They are simply ideas used in models to help explain certain concepts. You don't even understand them to begin with, so why do you bring them up?

What exactlly is a "local optimum" in the context of a "fitness landscape?"

Rocketdodger, don’t superimpose your lack of understanding of what a “local optimum” and “fitness landscape” are on me. If you want to understand what a fitness landscape is, consider how this concept works in ev. There are 4^G points on the fitness landscape surface. Each one of these points is one of the 4^G possible genetic sequences. Each one of the genetic sequences has a number of mistakes associated with the sequence and the selection conditions (the environment). You can construct the fitness landscape by computing the number of mistakes for all 4^G possible points on the fitness landscape. This surface has peaks and valleys which are represented by the numbers of mistakes. The highest peaks have zero mistakes and the lowest valleys could have G number of mistakes. A local optimum occurs when a population is at a particular peak. Any movement of the population away from this peak reduces the population’s fitness to reproduce. The selection conditions restrain the population from moving from the peak. Note that a local optimum does not necessarily coincide with zero mistakes.

That’s pretty much how the sort works rocketdodger. When you plug in the numbers like Dr Schneider did, you can watch how this process works mathematically.

Except that Schneider's program is an extremely limited model that is only supposed to show the ability of populations to evolve control mechanisms for their genomes. I still don't know how you are applying it to mutation and selection in general. As Paul says, it doesn't even really include the ability to use truly different selective pressures at once.

I think you would get an argument from Dr Schneider about the limitations of ev. In his peer reviewed and published article on ev, he used the results to estimate the evolution of a human genome. I haven’t seen any evolutionists criticize Dr Schneider’s mathematically illogical conclusion from his model. What ev does accurately simulate is the affect of different selection conditions on the sorting of mutations. This is why it takes huge numbers of generations to evolve binding sites on all but the tiniest genomes. That’s the lesson that Dr Schneider’s model teaches. Now rocketdodger, if you want to try to define different selection conditions that will lead to faster sorting of mutations, have at it.

That’s not correct rocketdodger. Every mutation has affect on the process but not nearly as much as the number of selection conditions.

What does this have to do with what I wrote?

It has everything to do with how mutation and selection actually works.

You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.

We will see.

We all look forward to this. Why do I have the feeling we are in for a long, long wait?

These scientists are trying to isolate and identify the mutations that give resistance to particular drugs. Why would they introduce other selection pressures which would interfere with what they are trying to identify? They grow their populations in incubators with plenty of resources needed by the population and introduce the drugs slowly so as not to kill the entire population.

Okay, I'll take your word that they've got it completely under control. Who's got it under control in the real world?

Paul, you do understand that in vitro measurements of evolution don’t include immune responses whereas the in vivo response does?

Paul, you are not going to make a point here by being cute. Ev is a collection of equations and conditional statements which produces data from its sorting/optimization algorithm which simulates the mutation and selection process. Dr Schneider’s equations are there, I have seen the code and it does a good job of simulating how the mutation and selection process works.

And you're not going to make a point by saying "Ev does present the math." in response to my statement "Presumably you have mathematics to show that in the real world the situation is such that only certain (unspecified) biological mechanisms could have evolved in the time available, while other extant mechanisms could not have evolved." Note how I use the term "real world."

Paul, you are the one claiming that biological mechanisms somehow evolved. Ev does not represent the evolution of binding sites. Ev represents the evolution of sequences of bases that satisfy the conditions imposed by Dr Schneider’s selection conditions. Ev demonstrates how slow a mutation/selection sorting algorithm performs when you have more than a single selection condition. That’s the “real world” which ev demonstrates. Anything else you claim about ev including some weird function associated with these sequences of bases is nonsense.

Stop being silly Paul, there is no function being evolved in ev. There are only sequences of bases which satisfy the selection conditions determined by matches to the weight matrix evolving in ev. Of course you can claim that ev is evolving real binding sites, then you can explain to us what the function of a binding site is for a gene that evolves binding sites. That would be an amusing story for you to tell us.

I didn't claim that Ev is evolving real binding sites, did I? I claimed that it is evolving a function, which is to match binding sites but no other positions on the chromosome. Then, when you turn off one or two selection conditions, it is not evolving that function. You have got to stop harping on my use of the word function, Alan.

2 : the action for which a person or thing is specially fitted or used or for which a thing exists : PURPOSE

I’ll stop harping on your use of the word “function” when you stop trying to describe what the three selection conditions in ev are doing. The selection conditions select for sequences of bases that satisfy those selection conditions and ev becomes very slow at satisfying all three selection conditions simultaneously on all but the tiniest genomes. That’s the mathematical fact of life that ev demonstrates about the mutation/selection sorting process. By the way, are you going to claim the evolution has a PURPOSE now?

You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.

Let's reword this so that it actually describes what happens:

You can run the numbers in Dr Schneider’s model. To evolve [the ability to distinguish binding sites from all other positions] for a 16k genome takes more than 5,000,000 generations while [to evolve matching at every position or no position] only takes at most 100 generations. Your hunch is wrong.

You're comparing apples and sardines.

Oh really? So when you give combination therapy to someone with HIV and some drugs target one part of the genome and other drugs target other parts of the genome has nothing to do with the analogous situation where some selection conditions in ev target particular parts of the genome and other selection conditions in ev target other parts of the genome in ev? Paul, you still don’t understand that mutation and selection is nothing more than a sorting/optimization problem and Dr Schneider and your algorithm does a very good job at demonstrating how this process works. It shows what happens when you have more than a single selection condition. It slows down the process profoundly.

Furthermore, these observations emphasize that sequential antiviral therapy with nucleoside analogues may allow the rapid selection of drug-resistant strains.

You know, you're emphasizing that simultaneous selection pressures make evolution more difficult, but you've cited mostly controlled lab experiments. Does your mathematical proof against evolution include the part where pressures can't happen sequentially in the real world?

Paul, simultaneous selection pressures make evolution more difficult in the real world, that is why combination therapy is used for HIV, TB, HBV, HCV, malaria, cancer, weeds,… Many of the citations I have posted are not laboratory studies; they are clinical/field studies. It is your mathematical model which shows how this works.

You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.

You mean like setting the mistake points for each condition? I tried it with the default settings, first with one at 10 and the other two at 1 -- on average 1000 generations to convergence. With 2 out of 3 set to 10, on average it took 700 generations to convergence. With all three set to 10, it took on average 650 generations to convergence.

Does this somehow help your theory out?

Set two of the three selection conditions to 0 so that you have only a single selection condition and see what happens to the generations for zero mistakes (perfect creature).

Delphi, the mathematics of mutation is not that complex, you have some understanding of the problem; otherwise you wouldn’t have posted the Wikipedia reference to fitness landscape.

Sorry, your rant here is totally irrelevant to my point.

So you want to draw a correlation between an intelligently designed computer program and a cell you claim came about by mutation and selection. What’s your point? Mutation and selection is not so complex, it is clear that it can’t do what you have claimed. It is mathematically impossible and your own citation to Wikipedia shows why. If my rant served to annoy you then it did the job.

Why don’t you tell us how a temperature change can transform hundreds, perhaps thousands of genes simultaneously?

How festive! Unfortunately, Halloween was last week.

I take it that you have withdrawn your claim that a temperature change is able to transform reptiles into birds. How have your studies going? Have you proved that insects evolve into insects yet?

Circles and Circles.

He believes evolution is wrong, therefore, it MUST be wrong.

If you are so certain, Kleinman, ignore the Jref, and submit your data to a reputable, peer reviewed publication.

You got it wrong Shalamar, its not circles and circles; it’s a spiral that you are watching as the theory of evolution goes down the drain. Why do you devalue JREF? You don’t think an educational forum is the appropriate place to debate such an issue?

It is not a correct interpretation if you want to claim that your argument has any scientific basis. Mutation and selection does not work that way either empirically or mathematically.

In no way does this answer refer to what I asked. I was asking if you would clarify a theoretical and admittedly tangential point for me. But of course you are correct: asking you to explain anything will never result in anything with a scientific basis. I withdraw my question, and let your refusal or avoidance of answering it speak for itself.

Kotatsu, we all know what your point is, you claim that entire genomes evolve simultaneously. The only problem for your view is that you have no mathematical or empirical evidence to support your view. On the other hand, I propose that evolving more than a single gene at a time profoundly slows the evolutionary process. I have mathematical and empirical evidence to support my view. Your so call science requires no mathematical or empirical evidence, my science has the mathematical and empirical evidence.

Until you present something that is measurable and repeatable, you present nothing more than mush. The hundreds of citations which I have posted identify explicitly what the selection pressures are, the target genes for the selection pressures and often times identify the specific loci and mutations required for adaptation to the selection pressures. So far, all you have presented is mush.

The fact that several different groups of animal have countered more or less the same set of selection pressures in different ways alone shows that the process is repeatable. When faced with the selection pressures I listed before (or a subset thereof, or a combination of these, or the subset, with unlisted ones), animals will evolve a way to get from tree to tree easier, for instance to get away from an arboreal predator. Some have solved this by flying, some by gliding, some by jumping, and so on.

But I will present you, again, with the Brassica example. When different diploid species of Brassica were cross-bred, polyploid progeny occurred. These were cross-bred again, according to certain patterns (1), for five generations, and the resulting polyploid hybrids are analogous to two species of natural hybrids. In five generations of inbreeding, the plants acquired several morphological and physiological changes, including changes in leaf shape and colour, branching patterns, number of side shoots, and differences in fertility. The genetic distance between the F5 generation and the F2 generation varied between 3.7% and 9.6%. The selection pressures included having to cope with two different copies of the same gene within the same genome, having to cope with sudden polyploidisation, and several other factors which are present for all plants, such as microbial and other parasitism, pathogens, and so on. The authors used 82-89 nuclear DNA probes to detect changes in the genome, and detected changes with 23-59 of these probes, indicating, again, that no specific genes were targeted.

There are of course more details in the paper, but as you never read details and instead only post stock answers and lies, I see no reason to elaborate further.

More of your “more or less” mush. Why should you be surprised that recombination and selection leads to morphological and physiological changes? What are you trying to prove? Are you trying to prove that polyploidy Brassica are still Brassica and that recombination can yield morphological changes, you have succeeded. If you are trying to prove that this is an example of mutation and selection then you have failed.

Kotatsu, you are trying to make connections where none exist. You don’t have selection pressures which would make these transformations.

How on Earth can you make such a categorical statement? Am I to understand that you believe that regardless of what group of animal is under study, the researcher never knows any selection pressures operating on that group? Regardless of what gene he/she is working with?

The relevant selection pressures would of course change depending on the gene, the organism, and other factors. The same selection pressures wouldn't necessarily operate on a EF-1α tree as on an 18S tree. And in trees based on other genes, it is often possible to be very specific on at least some of the selection pressures operating on the gene in that organism.

Just because you don't understand phylogenies --- and this is becoming abundantly clear --- doesn't mean that the people who work with them don't.

Just because you don’t understand how mutation and selection works doesn’t suddenly make your phylogenic trees true. You have no mechanism to allow transformations like these, mutation and selection simply can not make these types of transformations. The mathematics of mutation and selection shows this and the empirical evidence of mutation and selection shows this. I don’t have to use your kind of “more or less” terminology, I can post mathematical and empirical data which shows that evolving more than a single gene at a time becomes profoundly slow by mutation and selection.

Kotatsu, you are in denial. Mutation and selection is not an incomprehensible process mathematically. If you ever come to understand that this process is nothing more than a sorting/optimization problem, you would realize that your belief system is wrong. The empirical evidence of how mutation and selection works verifies this. The pictures you draw are based on a mathematically impossible theory.

This, again, has nothing to do with my post. I was simply making the same observation as several other people have done before me, that your arguments are changing gradually as you are overwhelmed by evidence.

Your posts have nothing to do with mutation and selection. You can’t produce a measurable example which shows that multiple genes are evolving simultaneously by mutation and selection. On the other hand, I have presented hundreds of citations which show that combination selection pressures profoundly slow the evolutionary process and a peer reviewed and published model of random point mutations and natural selection which shows the same thing. The only thing that I am overwhelmed by is your lack of mathematical and empirical evidence for your view.

For some reason I don’t think I’ll ever pass your class in evolutionism or joobz’s class in alchemy.

No, I would imagine reading comprehension would be needed for both.

Perhaps I have a problem with reading comprehension but it is nothing to compare with your mathematical and scientific deficiencies, more or less.

Just stumbled over this:

Why don’t you tell us how a temperature change can transform hundreds, perhaps thousands of genes simultaneously?

Is there any reason why temperature change can't change a gene?

You didn’t know that this is how Delphi suggests that reptiles evolved into birds? He doesn’t seem to want to explain how this happens. Perhaps you want to take up the banner?

Temperature change can certainly change a gene; in fact, it would change the properties of many enzymes since the properties of these chemicals are strongly temperature dependent. Now do want to explain to us how mutation and selection can sort the mutations necessary to evolve so many genes simultaneously when the mathematical and empirical evidence shows that evolving more than a single gene at a time by mutation and selection becomes a profoundly slow process?

Ok I wrote a little simulation for use in investigating Kleinman's claim. I will post the source code on my website later today after I clean it up a bit.

The results show his theory to be wrong -- multiple pressures, of the same strength, eventually speed up the rate of evolution.

At first, it appeared as though Kleinman might be right -- adding selective pressures in low numbers really does slow the average rate of fixation way down. However, once a "critical mass" has been reached, adding pressures actually drives the rate back up. Eventually, with enough pressures, you get to a point where the average rate of fixation is equal to or faster than it is under only a single pressure.

“critical mass”, that sounds down right nuclear. Rocketdodger has mounted an E-bomb war head to his rocket in an attempt to hit the target. I think I am going to enjoy discussing this topic. This is going to be more fun that kjkent1’s string cheese theory of evolution.

Rocketdodger, you are going to post empirical examples of your model, won’t you? Oh, that’s right, you already have reptiles evolved into birds. Don’t forget to write your server software that speeds up as more users access the system.

The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions.

I don't see how this could be the point, since this is not what we were talking about. We were talking about how understanding and posting were two different things.

The mere fact that you're talking about a subject doesn't mean you know what you're talking about.

Are you going to start talking about beggaminases again?

If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly.

But why the hell would you want to do this ? What happens, instead, if you set two of the three conditions to a relatively low, non-zero value ?

We want to set two of the three selection conditions to zero because it demonstrates what happens to the rate of convergence for that single selection condition alone when compared to converging all three selection conditions simultaneously. Ev doesn’t quite handle relative selection pressure strengths quite correctly. In order to model this effect properly, the percent of the population which reproduces would have to vary with the selection pressure strength. As the model is written, the most fit half of the population is always allowed to reproduce no matter what the weight factors are.

That same behavior of mutation and selection is seen in reality in the numerous citations posted.

No, because you have not shown that those real-life examples have a number and relative strength of selection pressures that you can define.

Sure I have Belz, for example, HIV evolves resistance very rapidly to monotherapy while three drug therapy profoundly slows the evolution of the virus. HBV, HCV, TB, malaria, cancer, weeds,… all show the same effect. These examples often contain the specific mutations required to give immunity to the particular selection pressures.

Mutation and selection is simply a sorting/optimization problem.

You'd like that to be true, wouldn't you ?

It has nothing to do with what I would like, it has everything to do with what reality shows.

You can try to say that I don’t understand how mutation and selection works but I can produce data from a peer reviewed and published computer simulation of random point mutations and natural selection and hundreds of empirical examples which shows the same thing

Actually, that's precisely what I'm saying. You don't understand how mutation and selection works but you can produce data from a peer reviewed and published computer simulation of random point mutations and natural selection and hundreds of empirical examples which shows the same thing according to you.

Anyone who wants to run ev can and duplicate the data which shows how much more quickly a single selection condition evolves than all three selection conditions simultaneously. It’s very easy to cherry pick data which shows this as well, there is so much of it around. I do like cherries, don’t you Belz?

You mean like setting the mistake points for each condition? I tried it with the default settings, first with one at 10 and the other two at 1 -- on average 1000 generations to convergence. With 2 out of 3 set to 10, on average it took 700 generations to convergence. With all three set to 10, it took on average 650 generations to convergence.

Kleinman is talking about setting two out of three of them to 0. Then it'll converge in only a few generations. The problem, then, is that we're not evolving a creature who distinguishes bindings sites from other positions.

So what Paul? Give someone who suffers from HIV a PI and do you think that resistance to RTIs will evolve? All the ev sorting algorithm does in evolve sequences which satisfy the selection conditions whether they be one or three selection conditions simultaneously.

But why the hell would you want to do this ? What happens, instead, if you set two of the three conditions to a relatively low, non-zero value ?

Here are a few experiments:

standard model with all mistake points = 1: 662 gens

with all mistake points = 10 (should be same): 662 gens

with missed site points = 10 (heavier pressure): 316 gens

with two spurious binding points = 10 (different heavier pressure): 1267 gens

with just gene spurious binding points = 10: 889 gens

with just nongene spurious binding points = 10: 1034 gens

So changing the relative pressures has some fairly obvious effects. More pressure on missed binding sites results in faster convergence. More pressure against spurious binding sites results in slower convergence.

Now let's turn off pressures:

(a) with missed site points = 0: 1 gen

(b) with just gene spurious binding points = 0: 707 gens

(c) with just nongene spurious binding points = 0: 405 gens

(d) with both spurious binding points = 0: 6 gens

In cases (a) and (d), no distinction evolves between binding sites and other positions, so it takes no time to produce a creature with zero mistakes. Essentially, there are no mistakes.

In cases (b) and (c), a distinction between binding sites and other positions evolves, but only for a portion of the genome. Not surprisingly, if the portion that matters is larger (case b), it takes longer.

That’s correct, sorting on multiple conditions takes far longer than sorting on single conditions and the situation gets much worse as you lengthen the genome.

Kleinman's entire hypothesis is built on his introducing a software "bug" into ev. Using a zero value for any of the selection weights causes the population genomes to be filled with missing and/or spurious bindings, while simultaneously reporting a "perfect" creature. However, the program population is not actually evolving towards the known natural quality shared by the genomes of all independently living organisms: RSequence ~ RFrequency.

Really, I didn’t make Paul put the weight factor feature into ev. And I suppose I made hundreds of scientist post data which shows that combination selection pressures profoundly slow the evolutionary process by mutation and selection. Why don’t I post another citation which shows what kind of control I have over the scientific world since they publish the data for supporting my hypothesis.
http://aac.asm.org/cgi/content/full/48/6/2260?ck=nck

BILN 2061 is a novel, specific hepatitis C virus (HCV) NS3 serine protease inhibitor discovered by Boehringer Ingelheim that has shown potent activity against HCV replicons in tissue culture and is currently under clinical investigation for the treatment of HCV infection. The poor fidelity of the HCV RNA-dependent RNA polymerase will likely lead to the development of drug-resistant viruses in treated patients. The development of resistance to BILN 2061 was studied by the in vitro passage of HCV genotype 1b replicon cells in the presence of a fixed concentration of the drug. Three weeks posttreatment, four colonies were expanded for genotypic and phenotypic characterization. The 50% inhibitory concentrations of BILN 2061 for these colonies were 72- to 1,228-fold higher than that for the wild-type replicon. Sequencing of the individual colonies identified several mutations in the NS3 serine protease gene. Molecular clones containing the single amino acid substitution A156T, R155Q, or D168V resulted in 357-fold, 24-fold, and 144-fold reductions in susceptibility to BILN 2061, respectively, compared to the level of susceptibility shown by the wild-type replicon. Modeling studies indicate that all three of these residues are located in close proximity to the inhibitor binding site. These findings, in addition to the three-dimensional structure analysis of the NS3/NS4A serine protease inhibitor complex, provide a strategic guide for the development of next-generation inhibitors of HCV NS3/NS4A serine protease.

and

In the region of the active-site mutations, BI-1 and BI-2 are expected to project functional groups that are either structurally identical to or very similar to BILN 2061 when it is bound to the enzyme. Thus, it is expected that the losses in potency against the mutants are similar for all three serine protease inhibitors. The accurate comparison of the decrease (n-fold) in the potency of BI-2 to that of BILN 2061 is made difficult by the dramatically different potencies against the wild-type enzyme. Our results showed that any one of several single mutations results in a high level of resistance to BILN 2061. However, replicons containing either multiple mutations or single engineered mutations were still sensitive to IFN-α (Table 1 and 2), indicating that combination therapy similar to HIV treatment using several drugs with different functions and targets may help overcome drug-resistant mutations and control HCV infection.

 

[Belz...]

Well, the argument that Adequate and I are using only works if you have both a sufficient number of pressures and sufficient time for all of their targeted mutations to fixate. If the pressures are extremely lethal, the combination of them will kill off the population before any of that happens.

Which kind of begs the question why Kleinman uses this scenario in the first place -- of course there will be no evolution, the population is dead.

Well, all I was saying is that after a selection pressures kills off 90% of a population, suddenly 100% of the population has adapted to that pressure.

 

[Belz...]

No you haven’t shown how mutation and selection works mathematical, you posted a hunch. Dr Schneider’s model shows mathematically how mutation and selection works

Considering how you've addmitted that its conditions are CONTRIVED, and that it's a SIMULATION, I don't see how you can claim this. If Dodger made a program that illustrated his example, would it mathematically show anything to you ?

and I have posted hundreds of citations which show how mutation and selection works empirically.

Do you have a notepad file from which you copy-paste this bit in every one of your posts ?

So are you claim that sorting is done only by animate objects?

No, that's YOUR claim.

Mutation and selection is nothing more than a sorting/optimization problem

You wish. It'd make your position less frivolous.

While you are at it, why don’t your write server software that performs faster as more users access the server.

Now that's very interesting. If that's how you see evolution, then it's no wonder you misunderstand it so much.

The problem for evolutionists is that when there large genetic changes, they are catastrophic for the individual who has this large genetic mutation.

You're making sweeping statements, again.

I think you would get an argument from Dr Schneider about the limitations of ev. In his peer reviewed and published article on ev, he used the results to estimate the evolution of a human genome.

Can you spot the key word in your statement ?

Paul, you are the one claiming that biological mechanisms somehow evolved.

Actually the entire scientific community does. And "somehow" is misleading. But I wouldn't expect anything from someone who's idea of creation is based on two mutually-exclusive scenarios in a 3000-year old book.

Ev demonstrates how slow a mutation/selection sorting algorithm performs when you have more than a single selection condition.

Yes, it demonstrated how slow an ALGORITHM performs.

Paul, simultaneous selection pressures make evolution more difficult in the real world

Is this why we see new species arise ?

Oh, and did someone explain to you the difference between pressures all acting on a single gene and pressures acting on different ones ? Or are you going to argue that it's irrelevant, just like a pressure's relative strength ?

Mutation and selection is not so complex

Of course it isn't. But it's a lot more complex than you claim.

Just because you don’t understand how mutation and selection works doesn’t suddenly make your phylogenic trees true.

Yeah, I think they call those things "strawmen".

Are you going to start talking about beggaminases again?

Wow. I think that, so far, that's the Kleinman reply to a sentence of mine that has the LEAST to do with the sentence being replied to.

We want to set two of the three selection conditions to zero because it demonstrates what happens to the rate of convergence for that single selection condition alone when compared to converging all three selection conditions simultaneously.

Huh ? Are those selection pressures present or not ?

Ev doesn’t quite handle relative selection pressure strengths quite correctly.

Saved for posterity.

Sure I have Belz, for example, HIV evolves resistance very rapidly to monotherapy while three drug therapy profoundly slows the evolution of the virus.

Klein, you might know how many drugs are in use, but YOU HAVE NO IDEA HOW MANY OTHER PRESSURES ARE AT WORK.

It has nothing to do with what I would like, it has everything to do with what reality shows.

If that were true, you'd have given up your silly antics long ago.

 

[Belz...]

Anyone who wants to run ev can and duplicate the data which shows how much more quickly a single selection condition evolves than all three selection conditions simultaneously. It’s very easy to cherry pick data which shows this as well, there is so much of it around. I do like cherries, don’t you Belz?

Not your brand, no.

 

[Paul C. Anagnostopoulos]

I’ll stop harping on your use of the word “function” when you stop trying to describe what the three selection conditions in ev are doing.

They push the organisms toward evolving a gene that recognizes the binding sites but no other positions on the genome.

Ev represents the evolution of sequences of bases that satisfy the conditions imposed by Dr Schneider’s selection conditions.

And real evolution results in sequences of bases that satisfy the conditions imposed by the environment. Can you explain the difference to me?

By the way, are you going to claim the evolution has a PURPOSE now?

Keep your concepts straight, Alan. Evolution has no purpose. An evolved gene has a purpose, or better yet, to avoid the implication you bring up, it has a function.

Oh really? So when you give combination therapy to someone with HIV and some drugs target one part of the genome and other drugs target other parts of the genome has nothing to do with the analogous situation where some selection conditions in ev target particular parts of the genome and other selection conditions in ev target other parts of the genome in ev?

Correct, they have nothing to do with each other. In the first case, the therapies target multiple HIV genes. In the second case, there is only one gene.

In the first case, the multiple parts of the genome refer to multiple genes. In the second case, the multiple parts of the genome refer to one gene product's binding at multiple sites.

~~ Paul

 

[Paul C. Anagnostopoulos]

So what Paul? Give someone who suffers from HIV a PI and do you think that resistance to RTIs will evolve? All the ev sorting algorithm does in evolve sequences which satisfy the selection conditions whether they be one or three selection conditions simultaneously.

I give up, Alan. You insist on comparing two different evolutionary paths that produce different results as if one is simply an optimization of the other. Somehow we end up in the same place with one pressure instead of three. But clearly we end up in two different places.

No one is arguing that different results can require different amounts of time.

~~ Paul

 

[kjkent1]

Kleinman's entire hypothesis is built on his introducing a software "bug" into ev. Using a zero value for any of the selection weights causes the population genomes to be filled with missing and/or spurious bindings, while simultaneously reporting a "perfect" creature. However, the program population is not actually evolving towards the known natural quality shared by the genomes of all independently living organisms: RSequence ~ RFrequency.

Really, I didn’t make Paul put the weight factor feature into ev. And I suppose I made hundreds of scientist post data which shows that combination selection pressures profoundly slow the evolutionary process by mutation and selection. Why don’t I post another citation which shows what kind of control I have over the scientific world since they publish the data for supporting my hypothesis.

You didn't make up the weight factors. What you made up is the idea that ev operates to evolve a genome that matches the transcription factor when you set one of the selective weights to zero.

If you're not using ev in a manner which selects for both missing and spurious bindings, you're experiment is invalid, because what ultimately evolves is not a valid sequence logo. It's just a bunch of noise. You may choose to call that noise a different function, but it's not anything approaching a real genome.

Had Schnieder suggested that these other zero-weight selection conditions were valid, he wouldn't have been published. So, you need to lose this argument, because it's frivolous.

As for your posted examples, they all show that an overwhelming selective pressure, whether in vitro or in vivo, permits evolutionary change.

Now, do you have any evidence to show that natural environments never are subjected to a single overwhelming selective pressure over a generational period sufficient to permit an evolutionary change?

If you don't, then you LOSE, because the fossil record shows that such change has occurred in nature, which absent magic, could only have come about (according to you) through many overwhelming pressures operating sequentially.

 

[rocketdodger]

If you don't, then you LOSE,

He lost, and he knows it. Take a look at that last post of his! Not even so much as an attempt at an argument there -- nothing but nonsense and sarcasm.

He knows we got the better of him, and that we will easily refute anything he says, so now all he does is post jibberish and the repeated mantra of "that is what the mathematics and empirical evidence shows."

 

[kleinman]

Annoying Creationists

No you haven’t shown how mutation and selection works mathematical, you posted a hunch. Dr Schneider’s model shows mathematically how mutation and selection works

Considering how you've addmitted that its conditions are CONTRIVED, and that it's a SIMULATION, I don't see how you can claim this. If Dodger made a program that illustrated his example, would it mathematically show anything to you ?

Belz, virtually any mathematical model of mutation and selection will have to do some contrivance to model the selection conditions since in reality what selection pressures do is change the conformation of proteins. Dr Schneider’s contrived selection conditions still capture the consequence of multiple selection pressures on the sorting of mutations. Neither rocketdodger nor Adequate are going to successfully make a simulation that shows that n+1 selection pressures evolve more rapidly than n selection pressures that has any basis in reality. The mutation/selection sorting/optimization process simply doesn’t work that way.

and I have posted hundreds of citations which show how mutation and selection works empirically.

Do you have a notepad file from which you copy-paste this bit in every one of your posts ?

Nope, don’t need to, my 7th grade typing class was preparing me for this moment in time.

So are you claim that sorting is done only by animate objects?

No, that's YOUR claim.

Nope, that’s rocketwhomissesthetarget’s claim. Here, read this.
.

No. The environment is an inanimate object. How you think it could possibly sort anything is beyond me.

Mutation and selection is nothing more than a sorting/optimization problem

You wish. It'd make your position less frivolous.

What’s the matter Belz, don’t you like frivol?

While you are at it, why don’t your write server software that performs faster as more users access the server.

Now that's very interesting. If that's how you see evolution, then it's no wonder you misunderstand it so much.

So let’s see if we can understand how you view evolution. Things don’t evolve, they beggaminases. Now the theory of evolution is much clearer.

The problem for evolutionists is that when there large genetic changes, they are catastrophic for the individual who has this large genetic mutation.

You're making sweeping statements, again.

That’s right, I’m sweeping up the theory of evolution and throwing it into the dust bin.

I think you would get an argument from Dr Schneider about the limitations of ev. In his peer reviewed and published article on ev, he used the results to estimate the evolution of a human genome.

Can you spot the key word in your statement ?

The following quotes were taken from Dr Schneider’s blog web page: http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html
The following are Dr Schneider’s responses to a critique of his paper Evolution of biological information by Dr Stephen E Jones.

"Schneider's paper is misleadingly titled: "Evolution of biological information". But it is just a *computer* simulation. No actual *biological* materials (e.g. genomes of nucleic acids, proteins, etc) were used, nor does Schneider propose that his simulation be tested with *real* genomes or proteins

Actual biological materials were used to determine the original hypothesis. Read the literature: Schneider1986

It only becomes *real* biological information and random mutation and natural selection, when the simulation is tested in the *real* world, using *real* DNA, proteins, with *real* mutations and a *real* environment does the selecting. It is significant that Schneider does not propose this, presumably because he knows it wouldn't work.

You are very bad at reading my mind, I have considered doing this experiment. Given the right conditions, it WILL WORK. Do you have th gumption to do the experiment yourself? That's the way real science works! FURTHERMORE, if you read the literature, you will recognize that related experiments have been repeatedly done for 20 years. Look up SELEX.

In the rest of the paper he uses the single word "selection". I take this as a tacit admission that his model is not a simulation of *real* biological natural selection.

No. A rose is a rose by any other name. Selection is selection whether it be natural (generally meaning the environment of earth), breeding (by humans usually, though perhaps some ants select their fungi), SELEX or in a computer simulation. Of COURSE it is a simulation of natural selection! The paper would not be relevant to biology and would not have been published in a major scientific journal if it were not!

Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time":

So? Run the program slower if you want. Make one generation per 20 minutes to match rapid bacterial growth. THIS WILL NOT CHANGE THE FINIAL RESULT!

Well, when Schneider's simulation is actually tested with *real* "life" (e.g. a bacterium), and under *real* mutation and natural selection it gains information, then, and only then, would "creationists" be favourably impressed. But if they are like me, they would already be impressed (but unfavourably) that Schneider does not mention in his paper that his simulation should now be so tested in the *real* "biological" world.

1. The simulation was of phenomena in the "real" world.

2. Dr. Jones is invited yet again to do an experiment.

The following is a response Dr Schneider made to a statement made by David Berlinski.

Where attempts to replicate Darwinian evolution on the computer have been successful, they have not used classical Darwinian principles, and where they have used such principles, they have not been successful.

The ev program disproves this statement since it uses classical Darwinian principles and was successful.

Did you spot the key word Belz?

Paul, you are the one claiming that biological mechanisms somehow evolved.

Actually the entire scientific community does. And "somehow" is misleading. But I wouldn't expect anything from someone who's idea of creation is based on two mutually-exclusive scenarios in a 3000-year old book.

Belz, that’s a 3000 year old book and a peer reviewed and published model of random point mutation and natural selection and hundreds of citations that show that evolving more than a single gene by mutation and selection is a profoundly slow process, too slow for the theory of evolution to be mathematically or empirically possible.

Ev demonstrates how slow a mutation/selection sorting algorithm performs when you have more than a single selection condition.

Yes, it demonstrated how slow an ALGORITHM performs.

That’s right Belz, and the empirical data shows the same thing. That’s why the theory of evolution is mathematically impossible. Evolving more than a single gene simultaneously leads to a profoundly slow process.

Paul, simultaneous selection pressures make evolution more difficult in the real world

Is this why we see new species arise ?

Oh, and did someone explain to you the difference between pressures all acting on a single gene and pressures acting on different ones ? Or are you going to argue that it's irrelevant, just like a pressure's relative strength ?

Why don’t you post some citations about these new species, identify the selection pressures and the genes which have evolved and the mutations which have led to the new species? Kotatsu has tried to do this, more or less, actually, just less.

Mutation and selection is not so complex

Of course it isn't. But it's a lot more complex than you claim.

Is that why I can post hundreds of citations which show that combination selection pressures profoundly slow the evolutionary process and you have posted zero examples?

Ev doesn’t quite handle relative selection pressure strengths quite correctly.

Saved for posterity.

You can save it for whatever you want. Ev does handle selection pressures well enough to demonstrate that combination selection pressures profoundly slow the evolutionary process.

Sure I have Belz, for example, HIV evolves resistance very rapidly to monotherapy while three drug therapy profoundly slows the evolution of the virus.

Klein, you might know how many drugs are in use, but YOU HAVE NO IDEA HOW MANY OTHER PRESSURES ARE AT WORK.

What I do know is that all the other selection pressures at work do not have significant effect on the fitness of the virus to reproduce. Without the drugs, HIV is an early death sentence for whoever suffers from the disease. Why don’t you tell us what other selection pressures you know of against this virus?

It has nothing to do with what I would like, it has everything to do with what reality shows.

If that were true, you'd have given up your silly antics long ago.

What’s the matter Belz, don’t you like to frivol?

I’ll stop harping on your use of the word “function” when you stop trying to describe what the three selection conditions in ev are doing.

They push the organisms toward evolving a gene that recognizes the binding sites but no other positions on the genome.

So what again Paul? Evolving any of the three individual conditions alone give the appropriate sequences very quickly. It is only when you try to sort the mutations for all three conditions simultaneously that the sorting process becomes profoundly slow. That is the lesson that ev is demonstrating.

Ev represents the evolution of sequences of bases that satisfy the conditions imposed by Dr Schneider’s selection conditions.

And real evolution results in sequences of bases that satisfy the conditions imposed by the environment. Can you explain the difference to me?

Paul, I have been saying for the past year that ev does give a plausible simulation of how the mutation and selection process works. And what ev shows is that combination selection pressures profoundly slow the sort of mutations. Ev is analogous to how mutation and selection works in reality, single selection conditions evolve far more rapidly than combination selection pressures. That is what reality shows and that is what ev shows.

By the way, are you going to claim the evolution has a PURPOSE now?

Keep your concepts straight, Alan. Evolution has no purpose. An evolved gene has a purpose, or better yet, to avoid the implication you bring up, it has a function.

Paul, you put yourself in a logically impossible position. How do you select for something that has no function because until a gene exists, it has no function?

Oh really? So when you give combination therapy to someone with HIV and some drugs target one part of the genome and other drugs target other parts of the genome has nothing to do with the analogous situation where some selection conditions in ev target particular parts of the genome and other selection conditions in ev target other parts of the genome in ev?

Correct, they have nothing to do with each other. In the first case, the therapies target multiple HIV genes. In the second case, there is only one gene.

In the first case, the multiple parts of the genome refer to multiple genes. In the second case, the multiple parts of the genome refer to one gene product's binding at multiple sites.

Paul, ev has no function or purpose other than to sort the genomes based on the selection pressures imposed. You have three selection pressures targeted at three different parts of the genome. One selection condition is targeted at the nonbinding site region of the genome which removes sequences that match the weight matrix; another condition is targeted to the binding site region which forces sequences which match the weight matrix and a third condition which is targeted at the genes which eliminates sequences which match the weight matrix. This is analogous to targeting different sites on the HIV genome with different selection pressures. They have everything to do with each other because that is how the mutation and selection sorting/optimization process works mathematically and that is how it works empirically. If you target different parts of a genome with different selection pressures, it profoundly slows the sorting/optimization process.

So what Paul? Give someone who suffers from HIV a PI and do you think that resistance to RTIs will evolve? All the ev sorting algorithm does in evolve sequences which satisfy the selection conditions whether they be one or three selection conditions simultaneously.

I give up, Alan. You insist on comparing two different evolutionary paths that produce different results as if one is simply an optimization of the other. Somehow we end up in the same place with one pressure instead of three. But clearly we end up in two different places.

No one is arguing that different results can require different amounts of time.

Paul, the entire point of this discussion is that ev takes huge numbers of generations to evolve its three selection conditions for all but the tiniest genomes. Your theory calls for the transformations of huge numbers of genes in order for reptiles to evolve into birds. Your own model shows what happens to the sort/optimization when you have three selection conditions and real examples of mutation and selection show the same thing. I’ll post an example below which shows the difference between 1, 2, 3 and 4 selection conditions.

Really, I didn’t make Paul put the weight factor feature into ev. And I suppose I made hundreds of scientist post data which shows that combination selection pressures profoundly slow the evolutionary process by mutation and selection. Why don’t I post another citation which shows what kind of control I have over the scientific world since they publish the data for supporting my hypothesis.

You didn't make up the weight factors. What you made up is the idea that ev operates to evolve a genome that matches the transcription factor when you set one of the selective weights to zero.

You must have come up with this idea in one of your alternative universes because I have never said this. What I have always said is that each of the selection conditions selects for sequences of bases which satisfy the weight matrix. I don’t believe that ev evolves transcription factors even when you use all three selection conditions.

Now, do you have any evidence to show that natural environments never are subjected to a single overwhelming selective pressure over a generational period sufficient to permit an evolutionary change?

If you don't, then you LOSE, because the fossil record shows that such change has occurred in nature, which absent magic, could only have come about (according to you) through many overwhelming pressures operating sequentially.

Sure there are selective pressures that last over a generational period sufficient to permit an evolutionary change however the evolutionary change is not going to be accomplished by mutation and selection; it is just far too slow a process for transforming more than a single gene. The diversity in the fossil record is not due to mutation and selection, it is due to recombination and selection, just as we see great diversity in dog and cat population from recombination and selection. Mutation and selection can not accomplish these types of changes in so few generations; mutation can not be sorted that quickly.

So how does mutation and selection work? Here is another citation which shows how this phenomenon works.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1681928

More than a decade ago, it became apparent that treatment of HIV infection with only 1 antiretroviral agent was associated with the rapid development of resistance.[1] Clinical trials conducted at that time showed that combining 2 antiretroviral agents improved virologic and immunologic responses, compared with use of a single agent. Accordingly, 2-drug combination antiretroviral therapy became the standard of care to maintain viral suppression and minimize the emergence of resistant strains and, thereby, reduce the risk of disease progression and death. Subsequent experience and clinical trials showed that 3-drug combinations were substantially more effective than 2-drug combinations. Recommended 3-drug regimens of highly-active antiretroviral therapy (HAART) generally include 2 nucleoside or nucleotide analog reverse transcriptase inhibitors (NRTIs), plus 1 nonnucleoside analog reverse transcriptase inhibitor (NNRTI) or 1 protease inhibitor (PI).

and

When given as initial HAART, 4-drug regimens have shown promising preliminary results in recently completed studies as well as ongoing, comparative trials.[40,52]

Hey rocketwhomissesthetarget, better tell these scientists not to use too many selection pressures, they may start accelerating the evolution of the virus.

 

[Paul C. Anagnostopoulos]

Paul, I have been saying for the past year that ev does give a plausible simulation of how the mutation and selection process works. And what ev shows is that combination selection pressures profoundly slow the sort of mutations. Ev is analogous to how mutation and selection works in reality, single selection conditions evolve far more rapidly than combination selection pressures. That is what reality shows and that is what ev shows.

Then stop telling me that Ev only results in sequences of bases that satisfy selection conditions, rather than resulting in a genetic function. Make up your mind.

Paul, you put yourself in a logically impossible position. How do you select for something that has no function because until a gene exists, it has no function?

Indeed, selection cannot operate on something that has no function. But genetic drift can.

Paul, ev has no function or purpose other than to sort the genomes based on the selection pressures imposed.

I agree. But the gene that evolves in Ev does have a function. Otherwise there would be nothing for the selection pressure to press against.

You have three selection pressures targeted at three different parts of the genome. One selection condition is targeted at the nonbinding site region of the genome which removes sequences that match the weight matrix; another condition is targeted to the binding site region which forces sequences which match the weight matrix and a third condition which is targeted at the genes which eliminates sequences which match the weight matrix. This is analogous to targeting different sites on the HIV genome with different selection pressures.

I disagree.

Paul, the entire point of this discussion is that ev takes huge numbers of generations to evolve its three selection conditions for all but the tiniest genomes.

And yet you cannot present the math that shows:

[latex]$\mathit{huge number of generations} = \mathit{too long}$[/latex]

You must have come up with this idea in one of your alternative universes because I have never said this. What I have always said is that each of the selection conditions selects for sequences of bases which satisfy the weight matrix. I don’t believe that ev evolves transcription factors even when you use all three selection conditions.

What does it have to do with belief? Ev certainly does not evolve biological transcription factors. It evolves an abstraction of one. Nevertheless, the simulated gene has a function: to match the binding sites but no other positions.

Except when one or two of the mistake counts are zero, in which case the simulated gene has a different function.

~~ Paul

 

[kjkent1]

What does it have to do with belief? Ev certainly does not evolve biological transcription factors. It evolves an abstraction of one. Nevertheless, the simulated gene has a function: to match the binding sites but no other positions.

Except when one or two of the mistake counts are zero, in which case the simulated gene has a different function.

~~ Paul

For clarification: the "different" function, you refer to above, i.e., when a mistake count is zero, has no relationship to any known genetic behavior, as is the case when all three mistake counts are set to non-zero values.

Correct?

 

[CFLarsen]

You didn’t know that this is how Delphi suggests that reptiles evolved into birds? He doesn’t seem to want to explain how this happens. Perhaps you want to take up the banner?

Temperature change can certainly change a gene; in fact, it would change the properties of many enzymes since the properties of these chemicals are strongly temperature dependent. Now do want to explain to us how mutation and selection can sort the mutations necessary to evolve so many genes simultaneously when the mathematical and empirical evidence shows that evolving more than a single gene at a time by mutation and selection becomes a profoundly slow process?

Whoa. That's not what my question was about.

My question wasn't about genes changing by mutation and selection.

My question was about genes changing by temperature change.

Now, why can't hundreds of genes change, if they are subjected to temperature change?

As I understand you, if one gene is changing, the others don't change, regardless of what happens.

What mechanism causes this to happen?

Are the genes interconnected in some way?

 

[Cardelitre]

Lots of posts from T'ai Chi. Still no definition of "complex." Still no acknowledgment that this is a problem with his argument. If you're lurking, do you find this intellectually dishonest?

Obviously, yes. But is that really surprising?

*back lurking*

 

[rocketdodger]

Ok I put up the source code at http://www.jedi-arts.com/code/jev.cpp

There is also a sample input file at http://www.jedi-arts.com/code/data.txt


I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was

With a little experimentation you should be able to get a large number of pressures down to less than three times as slow as a single one (I have done it many times today while searching for that elusive prize of a combination). If you get better results, please post the parameters!

Also if you have any questions just ask. The source code should be pretty explanatory, though.

I can put a windows executable at that site if anyone desires it.

 

[Belz...]

Belz, virtually any mathematical model of mutation and selection will have to do some contrivance to model the selection conditions

Thank you, Klein. Welcome to sanity.

The mutation/selection sorting/optimization process simply doesn’t work that way.

Of course it doesn't. It's not strictly a sorting/optimisation process.

Nope, don’t need to, my 7th grade typing class was preparing me for this moment in time.

I can see you now, writing the same thing over and over on the blackboard.

"Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution. Hundreds of empirical examples showing that multiple selection pressures profoundly slow evolution..."

What’s the matter Belz, don’t you like frivol?

I just love it when an opponent chooses not to respond to another's point but resorts to "clever" sarcasm in order to draw attention away from it...

So let’s see if we can understand how you view evolution. Things don’t evolve, they beggaminases. Now the theory of evolution is much clearer.

Just to test you: what is the definition of "beggaminases" ?

That’s right, I’m sweeping up the theory of evolution and throwing it into the dust bin.

Translation: "I'm aware that I'm using logical fallacies, but that's all that's left, so now I'll use humour."

The following quotes were taken from Dr Schneider’s blog web page: http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html
The following are Dr Schneider’s responses to a critique of his paper Evolution of biological information by Dr Stephen E Jones.

BZzZT! Wrong answer! The key word was: estimate.

Belz, that’s a 3000 year old book and a peer reviewed and published model of random point mutation and natural selection and hundreds of citations that show that evolving more than a single gene by mutation and selection is a profoundly slow process, too slow for the theory of evolution to be mathematically or empirically possible.

So you ARE using the bibble ?

That’s right Belz, and the empirical data shows the same thing.

No, it doesn't. You've been consistently shown wrong on this. The fact that you're ignoring it changes nothing to the facts. Your interpretation of the empirical data is wrong, and your model doesn't represent reality. It doesn't matter how you word it. You are utterly wrong.

Why don’t you post some citations about these new species, identify the selection pressures and the genes which have evolved and the mutations which have led to the new species?

Err... why don't I not ? You're the one who's claiming that you can tell me how many selection pressures act on a certain gene. You have never done so. We HAVE seen new species. Hopefully you don't dispute that.

Is that why I can post hundreds of citations which show that combination selection pressures profoundly slow the evolutionary process and you have posted zero examples?

That has nothing to do with what I said, but I suspect neither will whatever drivel you will use to answer this sentence.

You can save it for whatever you want. Ev does handle selection pressures well enough to demonstrate that combination selection pressures profoundly slow the evolutionary process.

Aside from circular reasoning, how would you know ? Since it doesn't handle those pressures adequately, how can you tell that it handles them well enough ? Exactly HOW is that not a contradiction ?

What I do know is that all the other selection pressures at work do not have significant effect on the fitness of the virus to reproduce.

Again, saved for posterity.

You have just debunked yourself.

Other pressures exist, but are of too small relative intensity to have any substantial effect in the presence of the overwhelming pressure. Ergo, evolution.

 

[kleinman]

Annoying Creationists

Paul, I have been saying for the past year that ev does give a plausible simulation of how the mutation and selection process works. And what ev shows is that combination selection pressures profoundly slow the sort of mutations. Ev is analogous to how mutation and selection works in reality, single selection conditions evolve far more rapidly than combination selection pressures. That is what reality shows and that is what ev shows.

Then stop telling me that Ev only results in sequences of bases that satisfy selection conditions, rather than resulting in a genetic function. Make up your mind.

Paul who has the bicycle with the backwards facing seat because he has back peddled so much on what he claims about ev asks me to make up my mind. Well Paul, if you want to cling to the ridiculous notion that ev evolves something with genetic function, go for it. I’ll cling to my notion that all the ev sorting algorithm does is evolve sequences of bases which satisfy the selection conditions written for the model. My, my Paul, you really have some weird ideas about what ev does but that goes well with your belief in the theory of evolution.

Paul, you put yourself in a logically impossible position. How do you select for something that has no function because until a gene exists, it has no function?

Indeed, selection cannot operate on something that has no function. But genetic drift can.

Did you get your choice of colors for the paint which you use to paint yourself into a corner? So how do you get the evolution of a gene de novo? You remember what de novo means, from the beginning. There must have been a lot of drift in the primordial soup. Cyborg calls it the cruft theory of evolution.

Paul, ev has no function or purpose other than to sort the genomes based on the selection pressures imposed.

I agree. But the gene that evolves in Ev does have a function. Otherwise there would be nothing for the selection pressure to press against.

Paul, you have some weird ideas what the ev sorting algorithm does.

You have three selection pressures targeted at three different parts of the genome. One selection condition is targeted at the nonbinding site region of the genome which removes sequences that match the weight matrix; another condition is targeted to the binding site region which forces sequences which match the weight matrix and a third condition which is targeted at the genes which eliminates sequences which match the weight matrix. This is analogous to targeting different sites on the HIV genome with different selection pressures.

I disagree.

Make sure you click your heels together three times when you disagree with this.

Paul, the entire point of this discussion is that ev takes huge numbers of generations to evolve its three selection conditions for all but the tiniest genomes.

And yet you cannot present the math that shows:

hugenumberofgenerations = toolong

That’s what so much fun for me in this discussion, I don’t have to present the math; you and Dr Schneider have already done it for me.

Do you want to go back over your estimate of how many hundreds of millions of generations it would take to evolve your function on 96 loci for a population of 100k genomes yet you only have 500,000 generations to transform 150,000,000 loci differences on a 3 billion base genome to explain the differences between humans and chimpanzees. That shows that:
Hugenumberoflociintoofewgenerations = mathematicallyimpossibletheory

You must have come up with this idea in one of your alternative universes because I have never said this. What I have always said is that each of the selection conditions selects for sequences of bases which satisfy the weight matrix. I don’t believe that ev evolves transcription factors even when you use all three selection conditions.

What does it have to do with belief? Ev certainly does not evolve biological transcription factors. It evolves an abstraction of one. Nevertheless, the simulated gene has a function: to match the binding sites but no other positions.

Except when one or two of the mistake counts are zero, in which case the simulated gene has a different function.

So the function evolved in ev is an abstraction of a transcription factor. Once again you put your bicycle in reverse gear. Paul, you are the only person I know who has multiple reverse gears on your bicycle. Paul, tell us what the function of an abstraction of a transcription factor does.

What does it have to do with belief? Ev certainly does not evolve biological transcription factors. It evolves an abstraction of one. Nevertheless, the simulated gene has a function: to match the binding sites but no other positions.

Except when one or two of the mistake counts are zero, in which case the simulated gene has a different function.

For clarification: the "different" function, you refer to above, i.e., when a mistake count is zero, has no relationship to any known genetic behavior, as is the case when all three mistake counts are set to non-zero values.

Correct?

There you go Paul, explain to us how a single selection pressure in ev has no function yet the three selection pressures somehow do.

Also if you have any questions just ask. The source code should be pretty explanatory, though.

Just a couple of little questions, describe to us what the selection pressures are and give us a real example of what you claim the model represents.

You didn’t know that this is how Delphi suggests that reptiles evolved into birds? He doesn’t seem to want to explain how this happens. Perhaps you want to take up the banner?

Temperature change can certainly change a gene; in fact, it would change the properties of many enzymes since the properties of these chemicals are strongly temperature dependent. Now do want to explain to us how mutation and selection can sort the mutations necessary to evolve so many genes simultaneously when the mathematical and empirical evidence shows that evolving more than a single gene at a time by mutation and selection becomes a profoundly slow process?

Whoa. That's not what my question was about.

My question wasn't about genes changing by mutation and selection.

My question was about genes changing by temperature change.

Now, why can't hundreds of genes change, if they are subjected to temperature change?

As I understand you, if one gene is changing, the others don't change, regardless of what happens.

What mechanism causes this to happen?

Are the genes interconnected in some way?

So I guess you don’t want to take up Delphi’s banner that a temperature change was the selection pressure that transformed reptiles into birds. That’s what my original comment that you quoted was about.

Temperature changes certainly change the conformation of enzymes and their catalytic properties. The reason why hundreds of genes can not change simultaneously is that the mutation and selection process is a sorting/optimization problem. You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene. If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2. If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100. That’s why you can’t evolve hundreds of genes simultaneously. CFLarsen, here are a couple of examples which demonstrate empirically what happens to the mutation selection process when you have more than a single selection pressure.
http://en.wikipedia.org/wiki/Pesticide_resistance

Pest resistance to a pesticide is commonly managed through pesticide rotation, which involves alternating among pesticide classes with different modes of action to delay the onset of or mitigate existing pest resistance.[9] Different pesticide classes may have different effects on a pest.[9] The U.S. Environmental Agency (EPA or USEPA) designates different classes of fungicides, herbicides and insecticides. Pesticide manufacturers may, on product labeling, require that no more than a specified number of consecutive applications of a pesticide class be made before alternating to a different pesticide class. This manufacturer requirement is intended to extend the useful life of a product.[citation needed]

Tankmixing pesticides is the combination of two or more pesticides with different modes of action in order to improve individual pesticide application results and delay the onset of or mitigate existing pest resistance.[10]

http://www.absw.org.uk/Briefings/insecticide_resistance.htm

Using high doses of insecticide should maximise kill of heterozygotes and this strategy was popular among theorists in the 1970s. But to be really effective, the dose was too high to be acceptable on either environmental or cost grounds. Another drawback was that uniform coverage of the crop was not assured. The high dose strategy could be revived though with transgenic plants if it is possible to maintain a high level of expression of the toxin gene. The other strategy is pyramiding which involves creating trangenic plants with genes for two different toxins. Insects resistant to one will be killed by the other, and vice versa. This provides a double hit strategy for seeing off heterozygotes and discouraging the spread of resistance genes. It also parallels the successful use of combination drug therapy in leprosy, TB and HIV/AIDS.

Combination selection pressures targeting more than a single gene profoundly slow the evolutionary process. That’s what the mathematics shows and that’s what the empirical evidence shows.

 

[rocketdodger]

Just a couple of little questions, describe to us what the selection pressures are and give us a real example of what you claim the model represents

The pressures are completely random, and each of them targets a single mutation. You can even set the relative fitness bonus per pressure if you wish, but that gets tedious pretty quick, so I added the ability to just set them all to a given fitness bonus.

The model is just a quick and dirty simulation of mutation and selection. It shows that additional selective pressures do not hinder the sorting mechanism like you claim it does. In particular, adding more and more pressures can easily bring the time to fixation per pressure down to within 200% of the time to fixation for a singly applied pressure. I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.

Needless to say, even less than 200% is not "profoundly" slowed, and is certainly not what you describe here...

You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene. If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2. If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100.

...and you claim to have a degree in engineering...

 

[kleinman]

Annoying Creationists

Just a couple of little questions, describe to us what the selection pressures are and give us a real example of what you claim the model represents

The pressures are completely random, and each of them targets a single mutation. You can even set the relative fitness bonus per pressure if you wish, but that gets tedious pretty quick, so I added the ability to just set them all to a given fitness bonus.

The model is just a quick and dirty simulation of mutation and selection. It shows that additional selective pressures do not hinder the sorting mechanism like you claim it does. In particular, adding more and more pressures can easily bring the time to fixation per pressure down to within 200% of the time to fixation for a singly applied pressure. I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.

Needless to say, even less than 200% is not "profoundly" slowed, and is certainly not what you describe here...

Random mutation and random selection, just what exactly are you modeling?

You can’t change hundreds of genes simultaneously by mutation and selection. Transforming two genes by mutation and selection simultaneously is a much slower process than transforming a single gene. If you have two genes evolving simultaneously with each gene needing only a single mutation and the probability of 1 in a million for the probability of each mutation, the probability of any member of the population getting both mutations simultaneously is (1/1,000,000)^2. If you are evolving a similar system with a hundred genes evolving, the probability for a member of that population getting all the proper mutations simultaneously is (1/1,000,000)^100.

...and you claim to have a degree in engineering...

Actually three degrees, BS, MS and PhD. Now if you are having trouble with the mathematics above, perhaps you should take it up with this author.
http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x

Resistance genes are generally assumed to be biologically less efficient than the normal susceptible type. For example, an enzyme may escape drug action by a mutation that alters the drug-binding site. As this mutation probably also affects its catalytic capacity, the mutation will be removed from the population by natural selection and their frequency in the naive, non-drug-treated, population will be determined by a mutation/selection balance (Hastings 1997; Koella 1998). If drugs are used in combination, then the frequency of parasites resistant to both drugs will be

very low. For example, if 0.1% are resistant to drug A and 0.005% are resistant to drug B, then parasites resistant to both will initially be present at a frequency of 0.1 x 0.05% = 0.00005% (assuming that the same gene cannot encode resistance to both drugs). Thus using drugs in combination from the outset may greatly increase the useful therapeutic lifespan of the drug, because lowering the starting frequency delays the point at which a significant amount of resistance emerges.

And

One important general point from the models is that use of combination therapy in their initial deployment is invariably better than introducing one drug alone, followed by introduction of the second-line drug once the first becomes ineffective (see, for example, Curtis & Otoo 1986; Smith 1990; Bonhoeffer et al. 1997; for malaria, helminths and bacteria, respectively).

And

If parasites reach high numbers within hosts, then spontaneous mutations to resistance may occur. Infections of P. falciparum may reach 10^11-10^12 individual parasites per host and it seems logical that a small subpopulation may have mutated to drug resistance (for example if the mutation rate to resistance is 10^-8 then there would be 1000±10 000 resistant parasites) which then expands to dominate the infection. This argument seems logically plausible and receives support from observations of humans treated with the antimalarial drug atovaquone, where an infection which was originally susceptible disappears below detectable levels before recrudescing as a resistant infection (Looareesuwan et al. 1996). Measurements of drug sensitivity in vitro before and after treatment show greatly increased levels of resistance in the recrudescent infection. It seems plausible that the same effects may occur in other parasites that reach high population numbers within a host. Once again the effect can be minimized or even eliminated by using drugs in combination. In the above example of 10^11 parasites, mutation rates to resistance of 10^-8, and assuming two drugs were used in combination, then resistance would arise in only 10^16 parasites, in effect rendering the frequency of spontaneous mutations negligible. The implications for the evolution of drug resistance are discussed in Lipsitch and Levin (1997) and White (1999 and references therein).

Since rocketdodger hasn’t give a real example of his simulation, I think it is worthwhile to review what Adequate said about his model.

The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And then Adequate goes on to say this:

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?

And

So far as I know, no-one has done the experiment.

and

and too bad you don’t have any empirical examples of your silly graph ...

As I have explained to you, I produced the model because I've not heard of this precise experiment being done.
Now we have rocketdodger’s silly model. Any chance you could give us a real example of your model rocketdodger.

 

[joobz]

Unfortuantely, kleinman speaks a completely different langauge than the rest of the posters here.

Any logical well thought argument presented will be met with an equally illogical snide comment which does nothing to actually refute the argument presented him.


I still have yet to see any attempt of him to explain why his model assumptions are valid. He hopes that by ignoring this point or claiming it is irrelevant will make it magically disappear. However, it is clear to everyone that his aviodance of this (and many other points) is equal to admitting his theory is destroyed.