Annoying creationists

[kleinman]

Annoying Creationists

Another evolutionist flocks to this thread yet fails to read the thread. What you say here is contradicted by an evolutionist written and peer reviewed model of mutation and selection and numerous real examples of this phenomena. Perhaps you advocate the return to monotherapy for the treatment of HIV?

No, it is not. It's just that you're too obtuse to comprehend it.

Well Thabiguy, perhaps you want to explain what is said in Wikipedia about the fitness landscape or is that also too obtuse.

When using multiple drugs to combat an illness, resistance is less likely to occur, because 1) the population is dramatically reduced, and so the chance of a favorable mutation occurring are reduced, 2) the selection pressure is not for the occurence of any individual trait, but for their combination. Because developping individual drug resistance no longer ensures survival, its individual selection pressure is effectively lowered.

Of course selective pressures reduce population, but what you are missing is what ev shows, it is much easier to evolve to a single selection pressure than to multiple selection pressures. That is what is being said in the Wikipedia reference to fitness landscape as well.

That's akin to trying to breed dogs by getting a rifle and shooting all wolves you can find, unless they happen to be white, making white wolves more prevalent - and then wondering why, if you instead shoot wolves unless they look like a poodle, white wolves do not evolve quite so readily. You might conclude that it's because multiple selection pressures slow down evolution, and everyone else will correctly conclude that you are an idiot who knows nothing about breeding dogs.

Another evolutionist who thinks recombination and natural selection works like mutation and selection. Would you get your evolutionary processes straight?

Multiple selection pressures in the real world don't work by killing organisms left and right unless they acquire several traits simultaneously (sometimes that happens and species usually respond to it by going extinct). Having better teeth is a survival advantage and increases fitness - there is a selection pressure. Another selection pressure is added when having better eyes is also a survival advantage and also increases fitness. It does not mean that not having better eyes suddenly makes everyone die. Nor does it mean that having better teeth no longer increases fitness unless the creature simultaneously has better eyes.

Obviously you haven’t read this thread since you would have seen the numerous references to multiple selection pressures besides combination antimicrobials such as combination pesticides, combination herbicides and combination rodenticides, all of which show that the evolution of resistant strains is slowed by the use of the combination selection pressures. You also haven’t studied the ev computer model of mutation and selection and you haven’t read the Wikipedia reference to fitness landscape. If you had, you would have some idea how mutation and selection really works.

You fail to comprehend this because in your distorted world, using another drug is adding another selection pressure. You ignore the fact that it is, first and foremost, global reduction of the fitness of all organisms in the population and that it is not independent, as it reduces selection pressures on other traits by no longer making them a significant survival advantage. That is not the case for multiple selection pressures in the real world that are actually independent.

Adding another drug when doing combination therapy is adding another selection pressure and does reduce the global fitness of the creature. Of course selection pressures are independent and their effects on reproduction when combined are not linear. If you had any idea how ev works, this would be obvious to you. Evolutionists should really be made to take entire mathematics courses rather than dumbbell math then perhaps they would have a chance to understand ev. If you think that multiple selection pressures in the “real world” behave differently, then show us mathematically and/or give us real examples of this otherwise, join the roster of mathematically incompetent evolutionists who think they understand the mathematics of mutation and selection.

 

[kjkent1]

What part of these bizarre speculations convinces you that theory of evolution has any truth?

I provided you with citations to peer-reviewed science and you call them bizarre speculations. You just keep proving my point over and over, that you're not interested in anything scientific. This is all about you trying to raise your self esteem.

Well, we can add something to your string cheese theory of evolution. You think that genetic material flows back and fourth between living things like the sloshing of the primordial soup. Nothing stops that flow, not homology, nothing stops that flow.

The evidence proves that horizontal gene transfer occurs. If you want to "believe" that it occurs due to divine intervention, be my guest. But, that's religion, not science. If you're a scientist, then you will seek to identify the processes giving rise to HGT, instead of denying the possibility because your belief system demands otherwise.

Where did all those genes arise from anyway?

Just turn off all of ev's selection pressures, and all those genes will arise istantly -- just like what must have occured at the time of abiogenesis, when no selective pressures existed.

After all, if it happens in ev, then it must be true, because as you have repeatedly stated, you are not the one discrediting Schneider's model, because that would prove that your goal is to obtain revenge from your perception that he has discredited you on his blog.

 

[Thabiguy]

Well Thabiguy, perhaps you want to explain what is said in Wikipedia about the fitness landscape or is that also too obtuse.

What particular part of the Wikipedia article about fitness landscape would you like me to explain?

 

[kleinman]

Annoying Creationists

What part of these bizarre speculations convinces you that theory of evolution has any truth?

I provided you with citations to peer-reviewed science and you call them bizarre speculations. You just keep proving my point over and over, that you're not interested in anything scientific. This is all about you trying to raise your self esteem.

Post the quote(s) from your peer-reviewed science that you think supports your point.

Oh yes, you are so right, this is all about raising my self esteem, you silly little gator. This has nothing to do with ev showing the theory of evolution to be mathematically impossible.

Well, we can add something to your string cheese theory of evolution. You think that genetic material flows back and fourth between living things like the sloshing of the primordial soup. Nothing stops that flow, not homology, nothing stops that flow.

The evidence proves that horizontal gene transfer occurs. If you want to "believe" that it occurs due to divine intervention, be my guest. But, that's religion, not science. If you're a scientist, then you will seek to identify the processes giving rise to HGT, instead of denying the possibility because your belief system demands otherwise.

So your latest proposal is that horizontal gene transfer is what evolved us from our primate precursor. Now you’ve added another dish to our red herring, string cheese and whine meal, a big bowl of sloshing primordial soup.

Where did all those genes arise from anyway?

Just turn off all of ev's selection pressures, and all those genes will arise istantly -- just like what must have occured at the time of abiogenesis, when no selective pressures existed.

Hey, what alternative universe are you in now?

After all, if it happens in ev, then it must be true, because as you have repeatedly stated, you are not the one discrediting Schneider's model, because that would prove that your goal is to obtain revenge from your perception that he has discredited you on his blog.

Now be careful, my self esteem is at stake. Could you pass me another bowl of primordial soup? Maybe the horizontal transfer of a few genes will help my self esteem problem.

Well Thabiguy, perhaps you want to explain what is said in Wikipedia about the fitness landscape or is that also too obtuse.

What particular part of the Wikipedia article about fitness landscape would you like me to explain?

Post it again? Ok, Thabiguy, here it is for about the 5th time.

Fitness landscapes are often conceived of as ranges of mountains. There exist local peaks (points from which all paths are downhill, i.e. to lower fitness) and valleys (regions from which most paths lead uphill). A fitness landscape with many local peaks surrounded by deep valleys is called rugged.

Apart from the field of evolutionary biology, the concept of a fitness landscape has also gained importance in evolutionary optimization methods such as genetic algorithms or evolutionary strategies. In evolutionary optimization, one tries to solve real-world problems (e.g., engineering or logistics problems) by imitating the dynamics of biological evolution. For example, a delivery truck with a number of destination addresses can take a large variety of different routes, but only very few will result in a short driving time. In order to use evolutionary optimization, one has to define for every possible solution s to the problem of interest (i.e., every possible route in the case of the delivery truck) how 'good' it is. This is done by introducing a scalar-valued function f(s) (scalar valued means that f(s) is a simple number, such as 0.3, while s can be a more complicated object, for example a list of destination addresses in the case of the delivery truck), which is called the fitness function or fitness landscape. A high f(s) implies that s is a good solution. In the case of the delivery truck, f(s) could be the number of deliveries per hour on route s. The best, or at least a very good, solution is then found in the following way. Initially, a population of random solutions is created. Then, the solutions are mutated and selected for those with higher fitness, until a satisfying solution has been found.

Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).

 

[Taffer]

Considering this is a thread about the mathematics of mutation and selection and you presented an example of recombination of selection, I’m not so sure you understand the difference.

Kleinman, you clearly do not know what recombination is. Recombination occurs during meiosis. It has nothing to do with selection. It is a phenomenon wherein portions of one arm of a chromsomal pair 'swap' with its neigbour. Again, this has nothing to do with modelling selection. The model I gave has nothing to do with recombination or mutation. It models the change in allele frequency over time. That is evolution. I know far better then you what the difference is.

Just so there is no confusion for the casual reader, both recombination and mutation are sources of variation in a population, which is one of the main premesis of evolutionary theory.

Here is where you confuse the mathematics of mutation and selection and the mathematics of recombination and selection.

Again, you obviously have no clue what recombination is. Both recombination and mutation are sources of variation in a population. I couldn't possibly have confused the two, because the model I gave doesn't deal with either.

There are far fewer genes and alleles than there are loci in a genome where random mutations occur.

Here you clearly do not know what an allele is. An allele is a specific sequence of DNA (be it a single basepair or many basepairs) which is more common in the population then, if memory serves me, 0.5%. It is just one "form" of a sequence which is found in a population. Mutation and recombination both work in all parts of a genome, not just where genes are. A locus is just one specific location on a genome.

Hopefully I have cleared up your confusion in this matter.

The selection process for recombination works very quickly.

Please explain how selection works differently for variation gained by random mutation and variation gained through recombination. You might find this difficult, because there is no difference.

A hemoglobin S gene can form by mutation and the beneficial affect of this allele in certain environments can quickly propagate through the population by recombination and selection and give the results you describe.

Urg, kleinman, please don't use terms incorrectly when you don't know what they mean. Recombination does not propegate alleles throughout a population, breeding does. Selection leads to a change in allele frequency, yes, however.

However, combination therapy of HIV is an example of mutation and selection alone without recombination. The individual selection pressures from the combination therapy are discrete selection pressures that act and particular points on enzyme systems for the virus and can not simply be summed up.

Oh dear. Kleinman, do you have any idea what recombination is?

Anything can be summed up. Please explain how combination therapy of HIV is different from any other system. Hint: it isn't.

The selective advantage for hemoglobin S heterozygote in certain malaria endemic environments occurs because homozygote hemoglobin S have sickle cell disease, homozygote normal hemoglobin get malaria and heterozygote hemoglobin S get neither because of only slightly defective hemoglobin.

Yes, kleinman, I know. What is your point in telling me this? How does this affect my model? It doesn't. The model still works.

You have not shown a case where multiple selection pressures evolve more quickly than a single selection pressure.

That's because it is meaningless, as I've explained time and again, kleinman. If multiple selective pressures lead to stronger selection, then it's painfully obvious that it does. And since multiple selective pressures do lead to stronger selection, you do the math.

Another evolutionist flocks to this thread yet fails to read the thread. What you say here is contradicted by an evolutionist written and peer reviewed model of mutation and selection and numerous real examples of this phenomena. Perhaps you advocate the return to monotherapy for the treatment of HIV?

Kleinman, for the millionth time, HIV treatment has nothing to do with multiple selection pressures!

Kleinman, all you have shown in this thread is that you do not understand evolutionary theory, genetics, or biology. You do not know what recombination is, you do not know what an allele is, you do not know what selection is. I gave you your model, but now you claim it models "recombination", which is does not, rather then "mutation", which is it also does not. You also claim it doesn't model sickle cell enimia, which it does.

 

[kleinman]

Annoying Creationists

Considering this is a thread about the mathematics of mutation and selection and you presented an example of recombination of selection, I’m not so sure you understand the difference.

Kleinman, you clearly do not know what recombination is. Recombination occurs during meiosis. It has nothing to do with selection. It is a phenomenon wherein portions of one arm of a chromsomal pair 'swap' with its neigbour. Again, this has nothing to do with modelling selection. The model I gave has nothing to do with recombination or mutation. It models the change in allele frequency over time. That is evolution. I know far better then you what the difference is.

Just so there is no confusion for the casual reader, both recombination and mutation are sources of variation in a population, which is one of the main premesis of evolutionary theory.

That’s a very nice review of review. And note that recombination can not create new genes and that recombination with natural selection can cause the loss of alleles. Recombination and selection is a much, much more rapid process for giving variation in a population as seen with animal breeding than is mutation and selection. You don’t seem to understand this despite your schooling.

Here is where you confuse the mathematics of mutation and selection and the mathematics of recombination and selection.

Again, you obviously have no clue what recombination is. Both recombination and mutation are sources of variation in a population. I couldn't possibly have confused the two, because the model I gave doesn't deal with either.

And recombination and selection deals with alleles and does not increase the information content in the gene pool while mutation and selection does have the capability of increasing information in the gene pool but at an extremely slow rate. You would understand this if you studied the mathematics that ev reveals.

There are far fewer genes and alleles than there are loci in a genome where random mutations occur.

Here you clearly do not know what an allele is. An allele is a specific sequence of DNA (be it a single basepair or many basepairs) which is more common in the population then, if memory serves me, 0.5%. It is just one "form" of a sequence which is found in a population. Mutation and recombination both work in all parts of a genome, not just where genes are. A locus is just one specific location on a genome.

Hopefully I have cleared up your confusion in this matter.

The only thing you have cleared up is you have absolutely no idea of the mathematics of mutation and selection. Recombination can only make new combinations of linked genes by crossing over between their loci. You can create variation in the population but you can not create new genes. A mutation is a permanent heritable change in the genetic material usually defined as a change in a single gene (point mutation) or more broadly for any structural change in a chromosome. The mathematical behavior of these two mechanisms of variation is completely different. Recombination and selection involves alleles where as mutation and selection involves a change in a particular allele, usually at a single loci.

The selection process for recombination works very quickly.

Please explain how selection works differently for variation gained by random mutation and variation gained through recombination. You might find this difficult, because there is no difference.

Oh, the basic concept of selection for recombination and mutation may be the same, that is beneficial alleles and beneficial mutations enhance reproductive fitness. Where they differ is in the rate at which variations can be achieved. In the case of recombination, you can select alleles that give you Chihuahuas to Great Danes and a myriad of other breeds of dogs in only 5000 generations yet they are all still dogs. You have no mathematical way of explaining the transformation of a reptile genome to a bird genome in the number of generations available. Mutation and selection is far too slow a process and you don’t have a selection pressure to do this and multiple selection pressures slow this process. Selection of alleles is very rapid; selection of mutations is a much, much slower process.

Stephen J Gould’s concept of punctuated equilibrium is only applicable to recombination and selection; it has no applicability to mutation and selection. Some day the differences in the mathematics of recombination and selection and mutation and selection will sink in with you evolutionists.

A hemoglobin S gene can form by mutation and the beneficial affect of this allele in certain environments can quickly propagate through the population by recombination and selection and give the results you describe.

Urg, kleinman, please don't use terms incorrectly when you don't know what they mean. Recombination does not propegate alleles throughout a population, breeding does. Selection leads to a change in allele frequency, yes, however.

Stop whining, I have to listen to your mathematically deficient understanding of recombination and selection and mutation and selection. Last I heard, genes in humans are formed by recombination (including genomes with the hemoglobin S gene) and if the a particular allele is beneficial, it will increase propagate, spread, proliferate, increase in frequency in the population. So your immature attempt at parsing words adds nothing to the discussion. And learn how to spell propagate. Once you do that, learn the differences in the mathematics of recombination and selection and mutation and selection. Then once you do that, do a google search with the following terms; combination "selection pressures" resistance and you will find a huge number of papers that show that combination selection pressures slow the evolution of resistant strains of a wide variety of different types of life forms. No need to parse words to try to make this point.

 

[Dr Adequate]

Well Thabiguy, perhaps you want to explain what is said in Wikipedia about the fitness landscape or is that also too obtuse.

There's an explanation of the article in the kleinman FAQ (see my sig) entitled "Why Lie #5 Is Funny".

You're welcome.

 

[Dr Adequate]

Do we know why kleinman is raving about recombination?

 

[Thabiguy]

Post it again? Ok, Thabiguy, here it is for about the 5th time.

You want me to explain how that is related to multiple selection pressures? All right.

Here, the population represents a set of solutions; every organism's genome is a particular solution. The problem to be solved is defined by the fitness function that maps a genome value to a number describing the fitness. We also need to be able to mutate the solutions, i.e. make small changes in them. For genomes, this is straightforward. And, to be able to select for particular traits, we need a way to derive a trait from the genome: let's define function trait(g):{set of genomes} -> number, which describes how well the trait is expressed in an organism with the given genome.

Selection pressure means that an organism with a particular trait will have better fitness. In other words, the fitness function f(g) will generally increase when trait(g) increases. If there is only one selection pressure (for one single trait), then by definition the fitness won't depend on anything but that trait and we can therefore consider the fitness function f(g) to be a function of the trait: f(g) = F(trait(g)), where the derivative F'>0.

For multiple selection pressures (say n) the fitness function becomes a function of n variables: f(g) = F(trait-1(g), trait-2(g), ... , trait-n(g)) growing in all variables, i.e. with partial derivative dF/dx(i) > 0 for 1<=i<=n (this expresses the fact that there is actually a selection pressure for each trait).

A multi-dimensional graph of this fitness function with respect to small changes in the genome that correspond to these individual traits (assuming they are independent) is the fitness landscape. Allowing the genomes to mutate and selecting according to the evaluated fitness essentially means numerically differentiating the fitness function with respect to small changes in the genome and forcing the population to "climb up" the multi-dimensional slope of the fitness landscape to find local optima.

As long as the traits are independent, or in other words, a small change in the genome that affects one trait won't affect another trait, each time that a mutation affects a single given trait, the fitness function will change - this follows directly from the partial derivative being positive for that trait - therefore making it clear whether this is going "up" or "down" the slope and allowing to select accordingly. And as long as the selection pressures are independent ( F(trait-1(g),trait-2(g),...,trait-n(g)) = F1(trait-1(g)) + F2(trait-2(g)) + ... + Fn(trait-n(g)) ), the steepness of the slope depends only on the given trait and the rate of convergence is thus independent on the number of variables of the fitness function (=the number of selection pressures).

Your ad-nauseum-repeated examples where selection rate is slowed are not examples of the selection pressures being independent - combining drugs does not select for any resistance, but for universal resistance. It is akin to selecting for one big mutation that achieves resistance to all drugs simultaneously. This has nothing to do with natural selection with selection pressures for multiple traits, each of them independently enhancing the fitness.

... Hmm. Now that I think about it, why have I written all this? I don't expect Kleinman to understand it and I know of no-one else who would have trouble understanding what the fitness landscape article is about. I guess I should find a better way to manage spending my time.

 

[kleinman]

Annoying Creationists

Post it again? Ok, Thabiguy, here it is for about the 5th time.

You want me to explain how that is related to multiple selection pressures? All right.

And then you said this:

For multiple selection pressures (say n) the fitness function becomes a function of n variables: f(g) = F(trait-1(g), trait-2(g), ... , trait-n(g)) growing in all variables, i.e. with partial derivative dF/dx(i) > 0 for 1<=i<=n (this expresses the fact that there is actually a selection pressure for each trait).

And then you said this:

As long as the traits are independent, or in other words, a small change in the genome that affects one trait won't affect another trait, each time that a mutation affects a single given trait, the fitness function will change - this follows directly from the partial derivative being positive for that trait - therefore making it clear whether this is going "up" or "down" the slope and allowing to select accordingly. And as long as the selection pressures are independent ( F(trait-1(g),trait-2(g),...,trait-n(g)) = F1(trait-1(g)) + F2(trait-2(g)) + ... + Fn(trait-n(g)) ), the steepness of the slope depends only on the given trait and the rate of convergence is thus independent on the number of variables of the fitness function (=the number of selection pressures).

I added the highlighting. What you call traits are not independent. There is no guarantee that a random mutation will move you only up or down slope. A mutation can be neutral and move you along an isocline. You can not uncouple the effects of multiple selection pressures. This is why the search on the fitness landscape is confounded and profoundly slowed when you have multiple selection pressures. You may have a genome that reaches a local optimum which is not a global optimal genome because any mutation from the genetic sequence reduces the fitness of the creature. The more selection conditions, the more dimensions the fitness landscape has and the selection conditions are not independent. Finding a path through a multidimensional fitness landscape becomes more and more difficult the more dimensions you have. Even if you have a single selection condition, you may not be able to evolve a global optimum because a local optimum stops the evolutionary process for that condition.

This is why Wikipedia includes the following statement.

Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).

The checking process is the mutations and the ability to reproduce is the measure of success in the search. Many selection conditions slow this checking process profoundly.

This is what ev shows, this is what the use of combination therapy for the treatment of HIV to prevent the evolution of resistant strains shows, this is what the use of combination therapy of TB shows, this what the use of combination pesticides shows, this is what the use of combination herbicides shows and the is what the use of combination rodenticides shows. They all show that multiple selection pressures slow evolution.

Your ad-nauseum-repeated examples where selection rate is slowed are not examples of the selection pressures being independent - combining drugs does not select for any resistance, but for universal resistance. It is akin to selecting for one big mutation that achieves resistance to all drugs simultaneously. This has nothing to do with natural selection with selection pressures for multiple traits, each of them independently enhancing the fitness.

Why don’t you tell us what these independent selection pressures are? We would all love to hear what these are.

... Hmm. Now that I think about it, why have I written all this? I don't expect Kleinman to understand it and I know of no-one else who would have trouble understanding what the fitness landscape article is about. I guess I should find a better way to manage spending my time.

I understand this enough to know there is no such thing as independent selection pressures. Of course you do know there are independent selection pressures and you are going to tell us what they are and give us real examples of these selection pressures.

 

[articulett]

Thabiguy--
Well, you summed it up really nicely, and it is written well. You can cut and paste it if you want to use it again. And I'm sure others may plagiarize. Remember, digital information is eternal, and though creationist thinking may not evolve, others of more brain plasticity may amble by and pick up a clue or two. (And to think, you wrote this very nice explanation without expecting heaven bonus points.)

 

[kleinman]

Annoying Creationists

Thabiguy--

Well, you summed it up really nicely, and it is written well. You can cut and paste it if you want to use it again. And I'm sure others may plagiarize. Remember, digital information is eternal, and though creationist thinking may not evolve, others of more brain plasticity may amble by and pick up a clue or two. (And to think, you wrote this very nice explanation without expecting heaven bonus points.)

You mathematically challenged evolutionists really like improperly interpreted mathematics. What you are having a hard time understanding is that any random mutation has the potential of moving that creature in any direction on the fitness landscape. You don’t have independent selection pressures that evolve only up or down slope on the fitness surface. Thabiguy has given you a new fantasy trip for you evolutionists to go on, but this one will go into the ever growing evolutionist trash can of bad ideas, like huge populations give marked acceleration of evolution, the mathematics is not there to support this idea.

 

[joobz]

What you are having a hard time understanding is that any random mutation has the potential of moving that creature in any direction on the fitness landscape.

Very Very good. This is true. And only those that are favorable(downhill in the landscape) to survival (or favorable enough) actually pass on the genes and propogate the good. Thank you for repeating back to all of us what we have tried so hard to get you to understand.

Your silly twofisted grip on the fistness landscape as verification of your delusions has been amusing to watch. Abandon this lie. It just highlights your inept understanding of science.

 

[delphi_ote]

Do we know why kleinman is raving about recombination?

The same reason he raves about pretty much anything: he doesn't understand it.

 

[Taffer]

That’s a very nice review of review. And note that recombination can not create new genes...

Yes it can, kleinman. Recombination is just another source of variation in a population, and it is this variation which leads to new genes. If mutations can cause new genes to arrise (which it can), so can recombination (which it does).

...and that recombination with natural selection can cause the loss of alleles.

What? No! Recombination does not lead to a loss of anything! Selection can lead to a loss of alleles. Genetic drift can lead to a loss of alleles. Hell, even mutation *might* lead to the loss of an allele (if every individual had the same mutation at that locus), although the likelyhood of that happening is tiny. But recombination never leads to a loss of genetic data. The data is still there.

Recombination and selection is a much, much more rapid process for giving variation in a population as seen with animal breeding than is mutation and selection. You don’t seem to understand this despite your schooling.

Actually, I think you'll find that I know this quite well. But what this has to do with your claim that my model uses "recombination and selection" is beyond me.

And recombination and selection deals with alleles and does not increase the information content in the gene pool while mutation and selection does have the capability of increasing information in the gene pool but at an extremely slow rate. You would understand this if you studied the mathematics that ev reveals.

I hope you understand, kleinman, that "information" is hardly ever used by evolutionary genetic scientists. Why? Because it is a meaningless concept. But for the sake of argument, variation is information. Recombination increases variation. Therefore, recombination increases information. QED.

The only thing you have cleared up is you have absolutely no idea of the mathematics of mutation and selection.

Recombination can only make new combinations of linked genes by crossing over between their loci.

Wrong. Recombination can, and does, occur inside a gene, thus breaking it. It can join new genes together, insert parts of one gene into another, duplicate genes to reduce evolutionary pressures, and much more. Recombination leads to increased variation within a population, and thus "increased information".

You can create variation in the population but you can not create new genes.

Why not? Mutation increases variation in the population, and that variation leads to new genes. How is the variation created through mutation different from the variation created from recombination? Hint: It isn't.

A mutation is a permanent heritable change in the genetic material usually defined as a change in a single gene (point mutation) or more broadly for any structural change in a chromosome.

Wrong. A mutation is simply the change to the genetic basepair sequence. This can occur in many ways, including, but not limited to, point mutations, indel mutations, inversions, duplications and insertions.

The mathematical behavior of these two mechanisms of variation is completely different.

Not really, but I won't get into that. Recombination equations are long and boring.

Recombination and selection involves alleles where as mutation and selection involves a change in a particular allele, usually at a single loci.

Mutations can occur which duplicate a large portion of a chromosome, kleinman. Mutation is not single basepair effecting only.

Oh, the basic concept of selection for recombination and mutation may be the same, that is beneficial alleles and beneficial mutations enhance reproductive fitness. Where they differ is in the rate at which variations can be achieved.

Yes, but does that matter? No. Because "recombination and selection" and "mutation and selection" are not two different things acting independently on evolution. What you really have is "recombination, mutation, reproduction (etc) and selection" which can be shortened to "variation and selection". It doesn't matter how variation arrises, what matters is that it is there. Variation caused by recombination is no different from variation caused by mutation. It is all variation.

In the case of recombination, you can select alleles that give you Chihuahuas to Great Danes and a myriad of other breeds of dogs in only 5000 generations...

You do not "use recombination". You use variation. The variation in the population came about through a combination of mutation, reproduction and mutation. Also, please note, that by and large recombination just moves genes around, although as I said earlier this isn't always the case. Once again, it matters not whence variation arose, only that it exists.

...yet they are all still dogs.

Can you explain what you mean by this? How are you defining what is a dog and what isn't? Be very specific.

You have no mathematical way of explaining the transformation of a reptile genome to a bird genome in the number of generations available.

Let us assume that we don't for the sake of argument. So? Does this mean it didn't happen? No, because it plainly did. There is more evidence that reptiles and birds shared a common ancestor then there is for us landing on the moon.

Mutation and selection is far too slow a process...

Not at all. Only if you take one form of mutation, point mutations, then perhaps it is. But mutations do not just act on a single locus.

...and you don’t have a selection pressure to do this...

Even if we can't, at the moment, describe a single selection pressure which caused birds to arise (the thought that it was only one is idiotic at best), does this mean it didn't happen? No. See above.

...and multiple selection pressures slow this process.

No they don't. Multiple selection pressures cause stronger selection, which increases the rate which allele frequences change over time. This is evolution.

Selection of alleles is very rapid; selection of mutations is a much, much slower process.

And here you show your fundamental lack of knowledge of genetics. An allele is just a specific sequence at a specific loci. New mutations give rise to new alleles. An allele is just like a name on a map. Some people have "new york" at that place, and some people have "washington" instead. Each different "name" at each location on the map which is present in a population is an allele. This can be a single basepair difference, or it can be many basepairs in length. A mutation which causes a basepair difference (i.e. all of them) at a specific locus generates a new allele.

Do you understand now?

Stephen J Gould’s concept of punctuated equilibrium is only applicable to recombination and selection; it has no applicability to mutation and selection.

No, kleinman, because there is no difference between "mutation and selection" and "recombination and selection". There is only "variation and selection".

Some day the differences in the mathematics of recombination and selection and mutation and selection will sink in with you evolutionists.

That isn't very likely, because this is all very well understood already, and it is known that different causes of variation all cause variation which is acted upon by selection. There is no difference.

Stop whining, I have to listen to your mathematically deficient understanding of recombination and selection and mutation and selection.

Since there is no such thing, I find this hard to believe. I say again, selection acts on variation in a population, not how that variation arose.

Last I heard, genes in humans are formed by recombination (including genomes with the hemoglobin S gene)...

No, genes in humans (and everything) arose through selection acting on variation.

...and if the a particular allele is beneficial, it will increase propagate, spread, proliferate, increase in frequency in the population. So your immature attempt at parsing words adds nothing to the discussion.

I'm not "parsing words", I'm pointing out that you are using the words incorrectly. And you plainly do not understand them, because you are comparing apples to appletrees. One is a fruit, and one causes fruit.

And learn how to spell propagate.

My spelling has nothing to do with the argument. Also, for everyone else, I'm fairly sure I have never used that word. Please point out where I have.

Once you do that, learn the differences in the mathematics of recombination and selection and mutation and selection.

I don't need to, because there is no such difference. There is only variation and selection, and both mutation and recombination give rise to variation. There is nothing different between the two "types" of variation. Variation is variation.

Then once you do that, do a google search with the following terms; combination "selection pressures" resistance and you will find a huge number of papers that show that combination selection pressures slow the evolution of resistant strains of a wide variety of different types of life forms. No need to parse words to try to make this point.[/SIZE][/FONT]

The first three results are as follows:

The incidence of trimethoprim resistance was correlated with changes in prescription behaviour in the Nottingham area from 1978-1985. The prevalence of trimethoprim resistance among Enterobacteriaceae isolated from patients with urinary tract infection rose from 5% to 15% of total strains examined. Strains resistant to trimethoprim but susceptible to sulfamethoxazole appeared from 1980 onward and represented 35% of the total trimethoprim-resistant strains examined in 1985. Co-trimoxazole (trimethoprim + sulfamethoxazole) has been generally available for prescription in the United Kingdom since 1969, whereas trimethoprim alone was released in October 1979. By 1983, prescriptions in the form of trimethoprim alone accounted for approximately 50% (in hospitals) and 15% (in the community) of total trimethoprim usage in the Nottingham area. Although the introduction of trimethoprim alone seems to have had only a minor effect on overall resistance levels, it has greatly increased the proportion of trimethoprim-resistant strains which are susceptible to sulfamethoxazole. This was particularly evident in strains of Proteus spp., in which 52% of the total trimethoprim-resistant strains were sulfamethoxazole-susceptible in 1985.

Source

Nothing in here about "multiple selection pressures slowing evolution".

WILD-TYPE reverse transcriptase has evolved for the survival of human immunodeficiency virus type 1 (HIV-1) by natural selection1. In contrast, therapy relying on inhibitors of reverse transcriptase by nucleosides like zidovudine (AZT) or dideoxyinosine (ddl), and by non-nucleosides like pyridinones or nevirapine2–6, may exert different selection pressures on this enzyme. Therefore the acquisition of resistance to reverse transcriptase inhibitors by selection of mutations in the pol gene7–15 may require compromises in enzyme function that affect viral replication. As single mutations are unlikely to confer broad resistance when combinations of reverse transcriptase inhibitors are used, multiple mutations may occur that result in further compromises. Certain drug combinations may prevent the co-existence of adequate reverse transcription function and multi-drug resistance (MDR). Unlike bacterial or eukaryotic drug resistance, retroviral drug resistance is conferred only by mutations in its own genome16 and is limited by genome size. Combining drugs directed against the same essential viral protein may thus prevent HIV-1 MDR, whereas the conventional approach of targeting different HIV-1 proteins for combination therapy may not, because genomes with resistance mutations in different HIV-1 genes might recombine to develop MDR17. Here we show that several mutations in the HIV-1 reverse transcriptase gene that confer resistance to inhibitors of this enzyme can attenuate viral replication. We tested whether combinations of mutations giving rise to single-agent resistance might further compromise or even abolish viral replication, and if multidrug-resistant viruses could be constructed. Certain combinations of mutations conferring resistance to AZT, ddl and pyridinone are incompatible with viral replication. These results indicate that evolutionary limitations exist to restrict development of MDR. Furthermore, a therapeutic strategy exploiting these limitations by using selected multidrug regimens directed against the same target may prevent development of MDR. This approach, which we call convergent combination therapy, eliminated HIV-1 replication and virus breakthrough in vitro, and may be applicable to other viral targets. Moreover, elimination of reverse transcription by convergent combination therapy may also limit MDR.

Source

Nothing in here about multiple selection pressures slowing evolution either. Please note that this paper is about multiple resistance development causing a functional change to a protein which inhibits viral reproduction.

The evolution of herbicide resistance within a weed population is based on selection pressure. The more frequently a herbicide is used, the more pressure placed on a weed population, and the sooner resistance will appear at a troublesome level in the population. Using alternative modes of action can reduce the potential for selecting resistant weeds by placing different selection pressures on weed populations. In a system relying only on glyphosate, a weed possessing a trait allowing it to survive glyphosate will rapidly increase in frequency. But if a second herbicide is used with glyphosate, this alternative herbicide may kill the weed with the glyphosate resistant trait and prevent it from increasing within the weed population. Theoretically this approach is sound and can reduce the potential for herbicide resistance.

Source

Nothing in here about multiple selection pressures slowing evolution. In fact, if you note the bolded section added by me, it actually says that increased selection pressure speeds up the evolution of resistance.

So, where exactly are all these "huge numbers" of papers?

 

[Taffer]

Do we know why kleinman is raving about recombination?

He mentioned it, and I called him on it, because he was showing a lack of understanding. Since then, it has become quite clear he doesn't grasp what any of these things are. Which isn't, in and of itself, a bad thing; people are allowed to not know things. But it's when they claim that they do, and that other people who actually do know do not, then one starts to look like an arse.

 

[Thabiguy]

There is no guarantee that a random mutation will move you only up or down slope. A mutation can be neutral and move you along an isocline. You can not uncouple the effects of multiple selection pressures. This is why the search on the fitness landscape is confounded and profoundly slowed when you have multiple selection pressures.

As the fitness function grows in all variables, a mutation that affects more than one trait can only be neutral if enhancing one trait means reducing other traits by the same amount. If this necessarily happens every time, then the traits are by definition inversely correlated, like trying to select for a long tail and for a short tail at the same time. If it doesn't happen necessarily but just by chance, then multiple selection pressures makes it less likely to happen: the isocline is a hyperplane and adding more dimensions makes it less likely to stay on this hyperplane by chance as there are increasingly more directions that lead away from it.

This is the case when there is actually a significant slope. If the slope is locally shallow, then it is useful to let the population's genomes spread around in search of a steeper slope.

You may have a genome that reaches a local optimum which is not a global optimal genome because any mutation from the genetic sequence reduces the fitness of the creature. The more selection conditions, the more dimensions the fitness landscape has and the selection conditions are not independent. Finding a path through a multidimensional fitness landscape becomes more and more difficult the more dimensions you have.

What a load of rubbish. The fitness function is scalar; the only criterion for selection is its simple number output. Saying that it's more difficult for a function to grow if it is a function of many variables is a good laugh. The fact that multi-dimensional slopes are too difficult for you to understand does not make them any more shallow or steep. The only thing that determines how fast the function will grow is the steepness of the slope, not the number of dimensions. If it's low - if the fitness function does not change much with changes of the genome - then the selection pressure for those changes is low.

But why bother with calculus? It's much better to use "common sense": multiple dimensions = whaaa...? = difficult = slow.

Even if you have a single selection condition, you may not be able to evolve a global optimum because a local optimum stops the evolutionary process for that condition.

A local optimum means that you've found a genome best adapted to the environment and any small change of the genome will lower the fitness of the organism. What you fail to comprehend is that adding more variables make it less likely that the evolution will stop in a local optimum. A local extreme in one dimension needn't be a local extreme in other dimensions; the population may develop the optimum beak size and not change it any more, but this doesn't prevent the change in the length of the tail feathers from improving fitness. As dimensions are added, there are more and more ways for the genome to change and to escape a partial extreme in a subset of dimensions in favor of a further increase of the fitness function.

With many variables, finding an optimum means that change in any trait decreases fitness. This can happen if the number of variables is relatively small - when selecting for a dog breed with, say, a dozen characteristics, then by the time all the traits are optimized, any further changes in those traits are undesirable and will be selected against by the breeders. But when the number of variables is much higher, there is virtually always a way to improve the population fitness and the evolution does not stop (it may slow down to a crawl if a particularly successful species evolves, as is the case with some insect species, but ultimately, changing environment will create new selection pressures anyway).

This is why Wikipedia includes the following statement.

Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).

This statement is included to explain the difference between optimization algorithms that improve solutions by looking for local changes that enhance their quality and deterministic algorithms that evaluate all solutions to find the best one (this scenario is inapplicable to evolution). It says that deterministic algorithms are impractical when there are too many discrete solutions (=genomes). It says nothing about the effectivity of the evolutionary algorithms with regard to the number of variables that the fitness function depends on (=multiple selection pressures). It is beyond my understanding how you can remain in a such a persistent denial of comprehension.

The checking process is the mutations and the ability to reproduce is the measure of success in the search. Many selection conditions slow this checking process profoundly.

No, that's just your misinterpretation. Mutations do not check the entire genome space to find the best solution. They check the local neighborhood to find the best enhancement of the solution. The measure of success in the search is the increase in the ability to reproduce. The number of the variables does not affect the rate of convergence; the steepness of the slope does. - Some basic experience with differential calculus would perhaps help you understand, or at least not confuse a function and its derivative.

Why don’t you tell us what these independent selection pressures are? We would all love to hear what these are.

Selecting for better teeth and for better claws allows the fitness function to independently increase by improving either trait. Selecting for better eyes and for a better immunity system allows the fitness function to independently increase by improving either trait. You can come up with a hundred examples of your own. - Practically all selection pressures are independent in that improving any individual trait will increase the fitness, except those that require several traits to occur simultaneously to increase the fitness. And the alleged impossibility of that is just the old irreducible complexity argument. Evolution does not need to "jump" across the flat fitness landscape to a distant mountain; instead, it finds an ascending path to this mountain through some of the many other dimensions.

 

[Thabiguy]

Why don’t you tell us what these independent selection pressures are? Wewouldall love to hear what these are.

Btw, are there people peeping over your shoulders as you type, are you under the impression that someone else here shares your... hmm, opinions - or do you just like to refer to yourself in the plural?

 

[Taffer]

Is there a functional limitation to the number of dimensions which can be run in fitness landscape simulations (i.e hardware limitations)? Or are high n dimension landscapes often run?

 

[Paul C. Anagnostopoulos]

Um, [random mutation and natural selection] as programmed in by an intelligent designer.

Ah, so now you're arguing that mutation and/or natural selection cannot arise in nature by naturalistic means? Or are you arguing that the specific type of mutation or selection in Ev might not occur in that exact fashion in nature?

~~ Paul