Genetic basis for human evolution

[KerrMetric]

Is the rate of divergence really that earth-shattering?

No it isn't. In fact its quite low.

 

[mark kennedy]

No it isn't. In fact its quite low.

It's not earthshattering, its impossible. When you get through the paper we can talk about why and how.

 

[shernren]

It's not earthshattering, its impossible. When you get through the paper we can talk about why and how.

And the mechanism that forbids it is?

 

[mark kennedy]

And the mechanism that forbids it is?

Actually, it is natural selection that forbids it. Natural selection can only preserve changes that provide a benefit and it cannot weed all of the deleterious effects out. The human genome has been completly mapped out and they have identified literally millions of SNPs and other mutations. What would you expect the ratio of beneficial effects to deleterious effects to be?

Grace and peace,
Mark

 

[KerrMetric]

Actually, it is natural selection that forbids it. Natural selection can only preserve changes that provide a benefit and it cannot weed all of the deleterious effects out.

This is not true Mark.

 

[shernren]

Actually, it is natural selection that forbids it. Natural selection can only preserve changes that provide a benefit and it cannot weed all of the deleterious effects out. The human genome has been completly mapped out and they have identified literally millions of SNPs and other mutations. What would you expect the ratio of beneficial effects to deleterious effects to be?

When you say "NS cannot weed out deleterious mutations" do you mean that empirically, theoretically, or both?

Theoretically, it is true from a mathematical standpoint that NS never completely removes deleterious mutations. It does however reduce them to negligible proportions, AFAIK. To draw an analogy, if we use an exponential equation to model the activity of a radioactive sample, the activity never goes to 0 and thus the sample never ceases to be radioactive. In actual fact however radioactive wastes would be safe after a certain number of half-lifes even though mathematically the activity is still positive - the activity has become negligible.

Empirically, I suppose you are pointing to something in the paper? (You can start citing it with me, you know. )

Your last ratio question? To be honest I don't know how I would begin to compute an answer. Beneficial or deleterious in comparison to what? Or in other words, how is the fitness function defined? To give a cliched example, the sickle cell hemoglobin mutation grants partial immunity, but causes sickle cell anemia - is that beneficial or deleterious, and how would you compute it?

And to be frank, within a certain range any number I give probably wouldn't be falsifiable. If I came up with the number 2:1, and you showed me a fitness function which "proved me wrong", I could probably easily adjust any few parameters to yield a new fitness function which would "prove me right".

 

[mark kennedy]

When you say "NS cannot weed out deleterious mutations" do you mean that empirically, theoretically, or both?

It is very empirical, scientists know for a fact that most mutations are neutral (it ranges around 98%) with the vast majority of the remainder being deleterious (harmfull).

Theoretically, it is true from a mathematical standpoint that NS never completely removes deleterious mutations. It does however reduce them to negligible proportions, AFAIK. To draw an analogy, if we use an exponential equation to model the activity of a radioactive sample, the activity never goes to 0 and thus the sample never ceases to be radioactive. In actual fact however radioactive wastes would be safe after a certain number of half-lifes even though mathematically the activity is still positive - the activity has become negligible.

Empirically, I suppose you are pointing to something in the paper? (You can start citing it with me, you know. )

Kerrmetric is studying the paper and I am anticipating a rather indepth expostion will be coming soon. I want to hold off on that for now, if you are interested I have two Quiet Posts submissions that explore this is a little more depth. There are a lot of issues here, Spontaneous mutation rates, genetic mechanisms, gene expressions. I don't want to rush into this, lets wait a while until Kerrmetric has a chance to offer his thoughts on the paper.

Your last ratio question? To be honest I don't know how I would begin to compute an answer. Beneficial or deleterious in comparison to what? Or in other words, how is the fitness function defined? To give a cliched example, the sickle cell hemoglobin mutation grants partial immunity, but causes sickle cell anemia - is that beneficial or deleterious, and how would you compute it?

You would have to consider what the mutation of a normal blood cell involves. Malaria is an infection so if the blood cells don't move properly through the veins and arteries it slows the spread of the infection. It does not improve immunity in any way shape or form. Other examples of benefical mutations have simular problems. For instance, there is one example of a beneficial mutation that is supposed to improve chances of survival from the HIV virus. There is an indel that creates a defective receptor in the T-Cells. The original HIV virus cannot latch on and inject the virus, but later strains can. This is another example where the immunity is not improved dispite the fact that a slight advantage results.

And to be frank, within a certain range any number I give probably wouldn't be falsifiable. If I came up with the number 2:1, and you showed me a fitness function which "proved me wrong", I could probably easily adjust any few parameters to yield a new fitness function which would "prove me right".

The effects of mutations are well known, there is a ton of stuff out in Cyberspace that clearly identify them. Most of them will do nothing at all (thank God for that) while the majority of the rest are deleterious. Adaptation would require an improvement of the brain, liver and various other vital functions. The human brain is not just 3 times bigger, it is actuall densor in the neural net. The frontal lobes are more developed and the Cerbral Cortex is much better developed.

Nothing in modern science provides a mechanism for making changes on this level. This paper offers the raw data but the genetic basis for human evolution is still unknown. The rate of change that would be reguired is too steap to be accumulated in such a brief period of time.

Grace and peace,
Mark

 

[shernren]

It is very empirical, scientists know for a fact that most mutations are neutral (it ranges around 98%) with the vast majority of the remainder being deleterious (harmfull).

But I am not asking whether most mutations are neutral or deleterious, and that is not what you said. I was asking what scientists observed about NS's ability to remove harmful mutations. Even if 99.999% of mutations were harmful, if NS was able to deplete their proportion so that they fell below the threshold of regular expression (so that 1 in 10,000, say, expressed that mutation) I would say that NS has done its job.

Kerrmetric is studying the paper and I am anticipating a rather indepth expostion will be coming soon. I want to hold off on that for now, if you are interested I have two Quiet Posts submissions that explore this is a little more depth. There are a lot of issues here, Spontaneous mutation rates, genetic mechanisms, gene expressions. I don't want to rush into this, lets wait a while until Kerrmetric has a chance to offer his thoughts on the paper.

Sure.

You would have to consider what the mutation of a normal blood cell involves. Malaria is an infection so if the blood cells don't move properly through the veins and arteries it slows the spread of the infection. It does not improve immunity in any way shape or form. Other examples of benefical mutations have simular problems.

Btw, I think I had better start using terms properly (and I'll admit I was fuzzy with them). When a person is homozygous for normal hemoglobin, well, then he's normal. When a person is heterozygous with one normal and one sickle allele, it's called sickle cell trait, and it does confer not just partial immunity but apparently better recovery from malaria. The blood cells rupture prematurely so that the plasmodium cannot finish its reproductive cycle, and the sickled proteins apparently are harder for the parasite to digest. In all other aspects the person is nearly normal. When a person is homozygous with 2 sickle alleles that's sickle cell anemia which we all know.

That's my whole point ... what is the fitness function being used? Or in layman's terms, "how do you define beneficial, exactly?" It's more complex than it seems, especially with that sickle cell trait noted above. Malaria is an endemic disesase where sickle cell trait is widespread, and there would be relatively more value in being partially immune to it, at the small risk of having a few sickled cells circulating in the blood - therefore sickle cell trait is good. But having children with another sickle-cell trait carrier would result in 1 out of 4 children having sickle-cell anemia - therefore sickle cell trait is bad. But if children with sickle-cell anemia die off younger, then the parents have more time to spend on each of the remaining children, thus increasing all their chances of surviving childhood - therefore sickle cell trait is good ....

For instance, there is one example of a beneficial mutation that is supposed to improve chances of survival from the HIV virus. There is an indel that creates a defective receptor in the T-Cells. The original HIV virus cannot latch on and inject the virus, but later strains can. This is another example where the immunity is not improved dispite the fact that a slight advantage results.

Which just shows that it is nearly meaningless to ask whether a mutation is "deleterious" or "beneficial" or "neutral" without taking into account the fitness function i.e. the environmental conditions and selective pressures.

The effects of mutations are well known, there is a ton of stuff out in Cyberspace that clearly identify them. Most of them will do nothing at all (thank God for that) while the majority of the rest are deleterious. Adaptation would require an improvement of the brain, liver and various other vital functions. The human brain is not just 3 times bigger, it is actuall densor in the neural net. The frontal lobes are more developed and the Cerbral Cortex is much better developed.

I interpreted your question as "what proportion of beneficial and deleterious mutations had been fixed into the human genome". Was I right to read it that way? Or (as it seems) not?

Is the human brain only 3 times bigger? Is that only over the past 5 million years? Taking a totally different tack, studying divergence rates of phenotypic expression (using the darwin unit, where divergence in darwins is the log of (measurement after divergence / measurement before divergence) and dividing it by 1 million years), that only amounts to something a little more than 0.2 darwins (off the top of my head, since 3 ~= e). Kenneth Miller in Finding Darwin's God reports that experimentally evolution rates have been measured in terms of thousands of darwins. If that's the maximum rate of evolution possible I don't see how evolution should have a problem with 0.2 darwins.

Nothing in modern science provides a mechanism for making changes on this level. This paper offers the raw data but the genetic basis for human evolution is still unknown. The rate of change that would be reguired is too steap to be accumulated in such a brief period of time.

Can you quantify this statement? Until you do it seems to be really just a matter of personal opinion.

 

[gluadys]

Actually, it is natural selection that forbids it. Natural selection can only preserve changes that provide a benefit and it cannot weed all of the deleterious effects out.

You still continue to avoid the fact that natural selection is a species-wide phenomenon. You are looking at the "balance-of-power" as it were of an invididual organism being born with some beneficial mutations and some deleterious mutations. Will the benefit outweigh the harm? And the answer in many cases will be "No".

But this is not what evolution is about. Evolution, and natural selection, apply to species, not to individuals. The result of natural selection is expressed statistically over the whole population.

Now tell me, how many of the deleterious effects of brain mutations in humans are expressed in more than 5% of the total human population?

Then tell me what harm it does to the species as a whole if a small percentage of the population suffers a serious affliction.

You might also explain why a deleterious mutation does not become more wide-spread in the population.

 

[mark kennedy]

You still continue to avoid the fact that natural selection is a species-wide phenomenon. You are looking at the "balance-of-power" as it were of an invididual organism being born with some beneficial mutations and some deleterious mutations. Will the benefit outweigh the harm? And the answer in many cases will be "No".

Cells are populations as well as fully developed organisms. Natual selection is kind of a balancing act in nature with certain populations dieing off while competing for limited resources. The thing they have finally realized is that it is not the neat linear progression, its runs in cycles.

But this is not what evolution is about. Evolution, and natural selection, apply to species, not to individuals. The result of natural selection is expressed statistically over the whole population.

Evolution is about changing alleles, if they test me to find if I'm a childs parent that's what they will look for. If they found say, three alleles that would be enough to prove I'm not.

Now tell me, how many of the deleterious effects of brain mutations in humans are expressed in more than 5% of the total human population?

Population genetics does not really interest me, presently I am interested in comparative genomics. Divergance, dispite the effect in human all tolled come to less then .1%. With canines it is like .15% dispite the fact that there are 30,000 distinct breeds and species of all shapes and sizes. The reason the variance is higher in dog populations is probably due to selective breeding. After a while inbreeding while produce fewing recombinations and result in defects, all pure breeds have problems with this. People who raise pure breeds will back breed them for this reason.

Then tell me what harm it does to the species as a whole if a small percentage of the population suffers a serious affliction.

By the same token how does a population benefit from a slight advantage in a small percentage of the population? That's the thing that makes this whole issue nearly unsolvable, these differnces are genome wide.

You might also explain why a deleterious mutation does not become more wide-spread in the population.

You might want to explain how beneficial effects from mutations do establish become wide-spread. Most of the adaptative traits expressed in population are due to recombinations of genes, the more alleles the better the chances of positive selection. Whether they are beneficial or not the chances of alterations of genes on an amino acid seqeunce level is unlikely to be fixed genome wide.

 

[mark kennedy]

But I am not asking whether most mutations are neutral or deleterious, and that is not what you said. I was asking what scientists observed about NS's ability to remove harmful mutations. Even if 99.999% of mutations were harmful, if NS was able to deplete their proportion so that they fell below the threshold of regular expression (so that 1 in 10,000, say, expressed that mutation) I would say that NS has done its job.

You describe natural selection as if it were a vestigal organ within the cell or in the metabolism. It's not, it's a concept based on the death of the less fit. Natural selection only preserves, it never produces anything. It only preserves based on the chances of survival of the populations with certain traits. Most of the time when extreme challenges in the environment favor only certain traits only certain ones will survive. Once the drought (or whatever) is over the recombination rate will tend to go back to the way it was.

Btw, I think I had better start using terms properly (and I'll admit I was fuzzy with them). When a person is homozygous for normal hemoglobin, well, then he's normal. When a person is heterozygous with one normal and one sickle allele, it's called sickle cell trait, and it does confer not just partial immunity but apparently better recovery from malaria. The blood cells rupture prematurely so that the plasmodium cannot finish its reproductive cycle, and the sickled proteins apparently are harder for the parasite to digest. In all other aspects the person is nearly normal. When a person is homozygous with 2 sickle alleles that's sickle cell anemia which we all know.

There are other variations of it as well if memory serves. If this was an imporved immunity like an adaptation of the T-cells then I would reconginize this as evolution. Sickle Cell is not the best way for populations to overcome malaria and sickle cell anemia causes terrible problems for people not living in areas with high levels of malaria.

That's my whole point ... what is the fitness function being used? Or in layman's terms, "how do you define beneficial, exactly?" It's more complex than it seems, especially with that sickle cell trait noted above. Malaria is an endemic disesase where sickle cell trait is widespread, and there would be relatively more value in being partially immune to it, at the small risk of having a few sickled cells circulating in the blood - therefore sickle cell trait is good. But having children with another sickle-cell trait carrier would result in 1 out of 4 children having sickle-cell anemia - therefore sickle cell trait is bad. But if children with sickle-cell anemia die off younger, then the parents have more time to spend on each of the remaining children, thus increasing all their chances of surviving childhood - therefore sickle cell trait is good ....

Think about what you are saying here because this mentality exists. In a lot of African cultures there is a great deal of importance put on passing you name down to your son. Because things are so hard they will have ten children in the hopes that maybe one son will survive to carry on the family name. One of their biggest problems is overpopulation and a common solution is to overpopulate. What is more, the burden put on the rest of the family when one of the members is sick is a drain on them emotionally and in other ways. Someone with sickle cell anemia will be a burden for quite some time, they will struggle with this their whole lives. If they survive malaria without the sickle cell trait they tend to have a greater immunity.

Which just shows that it is nearly meaningless to ask whether a mutation is "deleterious" or "beneficial" or "neutral" without taking into account the fitness function i.e. the environmental conditions and selective pressures.

It's the contention that mutations drive evolution that I am taking issue with. That is not what causes adaptation or positive selection of favored traits. The genetic mechanisms that do this by and large are fixed and quite stable. Natural selection is based on a now defunct theory of blending of characteristics, we now know that it is recombination of genes.

I interpreted your question as "what proportion of beneficial and deleterious mutations had been fixed into the human genome". Was I right to read it that way? Or (as it seems) not?

You read me right, I was emphasising the energetic costs of mutations. Alterations in the protein coding genes rarely derive a beneficial effect, in the rare events that they do they are never without consequences or defects. There are exception however, immune systems are known to be transposable (btw, sickle cell is not a change in the immune system).

The thing is, any alteration of the genetic code must be at least 99.99% as good as the previous one. This is very important when considering gross structural changes like gene duplications.

Is the human brain only 3 times bigger? Is that only over the past 5 million years?

Chimpanzee and human common ancestors supposedly split 5-6 Mya. The early Homo habilis skulls were only slightly bigger then modern apes 2.5 Mya. Homo erectus (Java man, Peking Man...etc.) had a pretty human looking skull and averaged a cranial capacity approaching that of modern humans. They emerge suddenly in the geologic record and continued until about .5 million years ago.

The thing is that the brain size grew seemingly overnight from being close to a modern ape to being close to modern human proportions. No explanation of what the genetic basis for this unprecedented expansion. Contrary to common misconceptions there is no neat lineal progressions, there are abrupt giant leaps in the fossil record.

Can you quantify this statement? Until you do it seems to be really just a matter of personal opinion.

I have several times but I don't mind doing it again. 35 million single nucleotides diverge between human and chimapzee genomes. According to evolutionary theory we diverged from the chimpanzee about 5 million years ago. That means that five nucleotides diverged every year (on average) for five million years. That is 100 nucleotides being fixed genome wide per generation (20-25 years) for five million years. That does not include the indels that are four times greater in size of the choromosomal rearrangements that are millions of nucleotides long.

It's all in the paper, with most of it found in the abstract. What is supprising about this is evolutionists act like this is exactly what they expected to find all along. There is a simple reason for this, if the divergance is too high to be accounted for by known genetic mechanisms that's the end of evolution as natural history.

What needs to be quantified is the per annum mutations being fixed at such an enormous level. Nothing like this has been directly observed or demonstrated, in fact the most likely effect from 98% of mutations is nothing at all. The vast majority are deleterious with these rare beneficial effects supposedly being the best explanation for human evolution.

I am not getting this from creationists, I'm am getting this directly from genetics research. It is evolutionary biology that has convinced me that special creation is the only viable explanation. I almost switched to a TE perspective then I discovered genetics. They can speculate about fossils but the DNA does not lie.

Grace and peace,
Mark

 

[shernren]

You describe natural selection as if it were a vestigal organ within the cell or in the metabolism. It's not, it's a concept based on the death of the less fit. Natural selection only preserves, it never produces anything. It only preserves based on the chances of survival of the populations with certain traits. Most of the time when extreme challenges in the environment favor only certain traits only certain ones will survive. Once the drought (or whatever) is over the recombination rate will tend to go back to the way it was.

Natural selection has almost nothing to do with the death of the least fit. The least fit don't have to die to drive natural selection. But their genes will be under-represented in the next generation compared the genes of the more fit. Variable reproductive success changes the relative proportions of alleles in the next generation. And I never asked natural selection to produce anything. What I did claim is that natural selection eventually ensures that deleterious genes are not expressed in a representative proportion of the population.

There are other variations of it as well if memory serves. If this was an imporved immunity like an adaptation of the T-cells then I would reconginize this as evolution. Sickle Cell is not the best way for populations to overcome malaria and sickle cell anemia causes terrible problems for people not living in areas with high levels of malaria.

And that, mark, is why the sickle-cell allele frequency is high in Africa, but is low in the modern population of Africans that were brought to the United States.

You read me right, I was emphasising the energetic costs of mutations. Alterations in the protein coding genes rarely derive a beneficial effect, in the rare events that they do they are never without consequences or defects. There are exception however, immune systems are known to be transposable (btw, sickle cell is not a change in the immune system).

The thing is, any alteration of the genetic code must be at least 99.99% as good as the previous one. This is very important when considering gross structural changes like gene duplications.

But is it valid to look at the energetic cost of mutating away from the modern human genome, and therefore jump to the conclusion that the energetic cost of mutating into the modern human genome is prohibitively high? Actually it's turning out to be a pretty interesting question: should we expect evolution to be time-reversible? Intuitively I'd say no, as a general rule ... without much in the way of quantifying my hunch.

You're right, sickle-cell trait doesn't really grant "immunity" to malaria in the sense of involving the immune system. However it does grant some "protection" against malaria, and having changed the term what I intended to say remains essentially unchanged.

It's the contention that mutations drive evolution that I am taking issue with. That is not what causes adaptation or positive selection of favored traits. The genetic mechanisms that do this by and large are fixed and quite stable. Natural selection is based on a now defunct theory of blending of characteristics, we now know that it is recombination of genes.

Natual selection works with any theory of inheritance which exhibits uneven reproductive success and copying with errors.

I have several times but I don't mind doing it again. 35 million single nucleotides diverge between human and chimapzee genomes. According to evolutionary theory we diverged from the chimpanzee about 5 million years ago. That means that five nucleotides diverged every year (on average) for five million years. That is 100 nucleotides being fixed genome wide per generation (20-25 years) for five million years. That does not include the indels that are four times greater in size of the choromosomal rearrangements that are millions of nucleotides long.

It's all in the paper, with most of it found in the abstract. What is supprising about this is evolutionists act like this is exactly what they expected to find all along. There is a simple reason for this, if the divergance is too high to be accounted for by known genetic mechanisms that's the end of evolution as natural history.

What needs to be quantified is the per annum mutations being fixed at such an enormous level. Nothing like this has been directly observed or demonstrated, in fact the most likely effect from 98% of mutations is nothing at all. The vast majority are deleterious with these rare beneficial effects supposedly being the best explanation for human evolution.

You seem to be thinking in a factory line paradigm. Evolution lines up all the divergent alleles that need to be fixed into the human genome on an assembly line and starts patching them in one by one. The second mutation doesn't get fixed until the first one does, the third doesn't until the second is, the fourth ... etc. You start working out "rates of mutation", and when you get a figure like 1 nucleotide every 0.2 years it seems preposterous because there's no way a nucleotide can be fixed in 0.2 years I agree. You are thinking of evolution as a sequential process, where every nucleotide has only 0.2 years to get fixed or else it won't root and the next nucleotide will take its turn and try to be fixed.

But here's my take on it: at the other extreme, each and every mutation has had 5 million years or 100,000 generations to be fixed into the genome - it's just that each and every mutation has had its go at it all at once. (Admittedly this oversimplifies things - not all mutations fixed are actually 5 million years old, some would have been more recent and thus had less time.) Doesn't seem so ridiculous now, does it?

What I want to know is if there is anything which actually prevents this scenario. I will be the first to admit that I'm no authority on genetics (I've said before that my views on origins come largely from the astrophysical point of view).

 

[mark kennedy]

Natural selection has almost nothing to do with the death of the least fit. The least fit don't have to die to drive natural selection. But their genes will be under-represented in the next generation compared the genes of the more fit. Variable reproductive success changes the relative proportions of alleles in the next generation. And I never asked natural selection to produce anything. What I did claim is that natural selection eventually ensures that deleterious genes are not expressed in a representative proportion of the population.

Well and good, that is an adequete description of what natural selection does. What it does not do is provide a comprehensive explanation for how genes at an amino acid sequence level are altered. Consider this, and bear in mind, what follows is not denied by either creations, ID scientists or evolutionists"

The building blocks of DNA are nucleotides compaosed of combinations of Adenine (A), cytidine (C), guanine (G), or uracil (U). The first part is either ribose (in RNA) or dexyribose (in DNA). The biggest difference between RNA and DNA is that ribose has uracil replaced by theymine (T). DNA is what stores the genetic information and expressing the language incolces decoding the polynucleotide language into the polypeptide language of proteins.

You with me so far? There are sixty-four possible combinaations of four bases taken three at a time (triplet codons). These possible permutations code for the 20 amino acids of life (I could list them if you are interested). There are 61 are used for amino acids and the other three are used as stop codons. This is what is vitally important to realize, when a codon is altered by one nucleotide chances are the reading frame will be shut down. If two are changed chances are that the reading frame will be shut down. If there are three changed in the proper sequence it can stay open. There is just one catch, it will later have to translate into a usefull protein.

As the RNA are translated from DNA to Proteins they are sent to the ribosome that effectively forges the proteins. That is the manufacturing analogy you noticed I am working from . What has to happen is the proteins have to fold together the way parts from an assembly line must fit together, if not there is a catabolic reaction and it's disolved in the cell.

And that, mark, is why the sickle-cell allele frequency is high in Africa, but is low in the modern population of Africans that were brought to the United States.

True, and that is also why sickle cell anemia is such a big health risk for African Americans in the States.

But is it valid to look at the energetic cost of mutating away from the modern human genome, and therefore jump to the conclusion that the energetic cost of mutating into the modern human genome is prohibitively high? Actually it's turning out to be a pretty interesting question: should we expect evolution to be time-reversible? Intuitively I'd say no, as a general rule ... without much in the way of quantifying my hunch.

The energetic cost is actually more then that, for instance, who needs half a heart? The same with modifications must produce more of a benefit then it costs. On a large scale we are looking at a three-fold expansion of the brain. This must include an expansion of the ability to produce normal blood cells at a more effecient rate. So peicemeal beneficial mutations don't really make any sense since this must be happening on a large scale and in symphony with other vital functions.

You're right, sickle-cell trait doesn't really grant "immunity" to malaria in the sense of involving the immune system. However it does grant some "protection" against malaria, and having changed the term what I intended to say remains essentially unchanged.

It's a slight advantage with evident and obvious energetic costs. It is not really adaptative, which the evolution of the brain and liver obviously would have had to be. Adaptation of the immune system happens regularly, we could not adjust to new viral strains if it didn't. Furthermore it would make immunization less then meaningless. Or greatest defense is improved fittness based on more efficient systems. Sickle-cell doesn't really do that and as you seem to realize, it has energetic costs that don't really improve fittness overall.

Natual selection works with any theory of inheritance which exhibits uneven reproductive success and copying with errors.

That is if, and only if, it it exibits improved reproductive success. Something else, since you mentioned copy with errors. One of the things that allows for relaxed functional constraint is when the change inhances the ablity of enzymes to eliminate transcript (copy errors). There real reason that transcript errors are not at zero is because it costs more then it benefits to produce this kind of efficency.

You seem to be thinking in a factory line paradigm. Evolution lines up all the divergent alleles that need to be fixed into the human genome on an assembly line and starts patching them in one by one. The second mutation doesn't get fixed until the first one does, the third doesn't until the second is, the fourth ... etc. You start working out "rates of mutation", and when you get a figure like 1 nucleotide every 0.2 years it seems preposterous because there's no way a nucleotide can be fixed in 0.2 years I agree. You are thinking of evolution as a sequential process, where every nucleotide has only 0.2 years to get fixed or else it won't root and the next nucleotide will take its turn and try to be fixed.

That is quite true and it is the germline mutations that are fixed. The sex cells are inheritable and truely transposable. The only other cells that are truely transposable are stem cells and brain cells. I'll let you consider that and we can talk about my point here some more.

But here's my take on it: at the other extreme, each and every mutation has had 5 million years or 100,000 generations to be fixed into the genome - it's just that each and every mutation has had its go at it all at once. (Admittedly this oversimplifies things - not all mutations fixed are actually 5 million years old, some would have been more recent and thus had less time.) Doesn't seem so ridiculous now, does it?

It actually becomes less tenable when taken into consideration the pleiontropic effects. The larger the change the more the effects are rachetted up. If you are talking about 100 changes fixed every generation you have to take into consideration the neutral and deleterious effects. Only in rare instances would they be beneficial and most adaptations come through recombinations, not SNPs, indels or chromosomal rearrangements.

What I want to know is if there is anything which actually prevents this scenario. I will be the first to admit that I'm no authority on genetics (I've said before that my views on origins come largely from the astrophysical point of view).

Genetics was the main selling point for me, but I am hardly an expert either. The scenerio you describe is not only viable, it is actually pretty reasonable. It's just that at the scale it would have had to happen it is anything but an explanation. The latest explanation is that neutral and slightly deleterious effects manage to escape natural selection. After a while new alleles are created and entered into the functional part of the genome and the protein coding genes.

When we finally get into the paper I'll show you how this is harder to do then we have been led to believe.

Grace and peace,
Mark

 

[gluadys]

[

Cells are populations as well as fully developed organisms.

A population is a population. It may be a population of paramecia, each of which is a single cell, or a population of beluga whales, each of which is an organism of trillions of cells.

The populations of tissue cells in the whales are of no evolutionary interest as they die with the origanism. Only germ line cells carry the whale genome to the next generation.

So I don't know what point you are trying to make. Whether we are talking about a unicellular or multi-cellular organism is irrelevant. We are still dealing with a reproductive population

Natual selection is kind of a balancing act in nature with certain populations dieing off while competing for limited resources. The thing they have finally realized is that it is not the neat linear progression, its runs in cycles.

“They”? Who is “they”? Biologists recognized this decades ago. Perhaps you mean that creationists are finally getting the message that evolutionary produces a bush-like phylogeny rather than a ladder?

The question of whether evolution selects species in competition as well as organisms within a species is one I haven’t looked into much, but it is probably of less importance than the intra-species competition that leads the species to change. What is importance here is the impact on variants within the human species.

Evolution is about changing alleles, if they test me to find if I'm a childs parent that's what they will look for. If they found say, three alleles that would be enough to prove I'm not.

No, evolution is about changing the distribution of alleles, not about changing the alleles themselves. Natural selection is the mechanism for changing the distribution of alleles. Your example again shows that you are focusing on individuals. To understand natural selection you must focus on the species as a whole because that is where natural selection is manifested.

Population genetics does not really interest me,

Which is why you have not learned to understand natural selection and continue to make erroneous assumptions about natural selection and evolution.

By the same token how does a population benefit from a slight advantage in a small percentage of the population? That's the thing that makes this whole issue nearly unsolvable, these differnces are genome wide.

I asked first. Are you now admitting that it does not harm the species if less than 5% of the population is afflicted with microcephaly or any other brain disorder you wish to name?

I will certainly grant that if only 5% of the population carries a beneficial mutation, the species as a whole has not yet benefited.

But then we come to the next question. Your “nearly unsolvable” problem is answered when you can answer that.

You might want to explain how beneficial effects from mutations do establish become wide-spread.

Again, I asked first. I will deal with your question when you have at least attempted to answer mine.

In fact, the answer to both questions is the same. The same process that restricts the spread of deleterious mutations into the population is responsible for making beneficial mutations wide-spread to the point of fixation.

Most of the adaptative traits expressed in population are due to recombinations of genes,

Irrelevant. Natural selection does not care if the mutation it is favoring originated in the current generation or 1,000 generations previously and has now been recombined into a favorable genetic pattern.

the more alleles the better the chances of positive selection.

Obviously. But once selection begins, the number of alleles will be reduced as only the most favorable are transmitted to future generations.

Whether they are beneficial or not the chances of alterations of genes on an amino acid seqeunce level is unlikely to be fixed genome wide.

Another bit of vocabulary to get straight. No gene is fixed genome-wide. The relevant concept here is not the genome—which is the total set of coding and non-coding sequences peculiar to the species, but the gene pool—which is the total number of the copies of the genome which exist in the germ line cells of a species’ population. Every gene is just one element in a genome. In each diploid cell, there are two copies of the species genome. In each gamete, there is one copy of the species genome. In the species as a whole there are as many (relevant) copies of the species’ genome as there are germ-line cells. This constitutes the gene pool.

Evolution is a change in the distribution of alleles across the gene pool. Natural selection is the major mechanism for changing this distribution.

So let’s go back to that last question. You have agreed that the distribution of deleterious mutations in a population is small. You have (I think) agreed that a species is not unduly harmed by a small proportion of its population being afflicted by such deleterious mutations.

Now, why does the distribution of such deleterious mutations tend to remain restricted to a small part of the population? After all, they seem to have the same opportunity to spread through the population as neutral and beneficial mutations. So why don’t they?


It may help to remember that the only way to pass a mutation from the first carrier to others is via reproduction.

 

[shernren]

Well and good, that is an adequete description of what natural selection does. What it does not do is provide a comprehensive explanation for how genes at an amino acid sequence level are altered. Consider this, and bear in mind, what follows is not denied by either creations, ID scientists or evolutionists"

The building blocks of DNA are nucleotides compaosed of combinations of Adenine (A), cytidine (C), guanine (G), or uracil (U). The first part is either ribose (in RNA) or dexyribose (in DNA). The biggest difference between RNA and DNA is that ribose has uracil replaced by theymine (T). DNA is what stores the genetic information and expressing the language incolces decoding the polynucleotide language into the polypeptide language of proteins.

You with me so far? There are sixty-four possible combinaations of four bases taken three at a time (triplet codons). These possible permutations code for the 20 amino acids of life (I could list them if you are interested). There are 61 are used for amino acids and the other three are used as stop codons. This is what is vitally important to realize, when a codon is altered by one nucleotide chances are the reading frame will be shut down. If two are changed chances are that the reading frame will be shut down. If there are three changed in the proper sequence it can stay open. There is just one catch, it will later have to translate into a usefull protein.

As the RNA are translated from DNA to Proteins they are sent to the ribosome that effectively forges the proteins. That is the manufacturing analogy you noticed I am working from . What has to happen is the proteins have to fold together the way parts from an assembly line must fit together, if not there is a catabolic reaction and it's disolved in the cell.

I also know what mitochondria, Golgi apparatus, chloroplasts and the endoplasmic reticulum do, as well as the four levels of protein structure, so I didn't really need that biochemistry primer, but thanks anyway!

What is happening is that you are assuming that protein modification has to "hit a sweet spot" for evolution to go forward. In one shot evolution has to go from this protein to that protein (both very well defined targets) so in your mind evolution can't do that and therefore it's an inadequate mechanism. But how are you so sure that other proteins won't work?

The energetic cost is actually more then that, for instance, who needs half a heart? The same with modifications must produce more of a benefit then it costs. On a large scale we are looking at a three-fold expansion of the brain. This must include an expansion of the ability to produce normal blood cells at a more effecient rate. So peicemeal beneficial mutations don't really make any sense since this must be happening on a large scale and in symphony with other vital functions.

Is there an actual physical principle that forbids natural selection to have synergistic effects, or is this simply a rehashed ID incredulity-of-low-probability argument?

It's a slight advantage with evident and obvious energetic costs. It is not really adaptative, which the evolution of the brain and liver obviously would have had to be. Adaptation of the immune system happens regularly, we could not adjust to new viral strains if it didn't. Furthermore it would make immunization less then meaningless. Or greatest defense is improved fittness based on more efficient systems. Sickle-cell doesn't really do that and as you seem to realize, it has energetic costs that don't really improve fittness overall.

To be frank Mark I don't think you're taking it from the point of view of people living in a land where malaria is endemic. In such places the advantages of having sickle-cell trait outweigh potential energetic costs. Malaria is a killer and anything that slows it down has big benefits.

[I don't like my terms unquantified - how would you propose to measure "energetic costs"?]

It actually becomes less tenable when taken into consideration the pleiontropic effects. The larger the change the more the effects are rachetted up. If you are talking about 100 changes fixed every generation you have to take into consideration the neutral and deleterious effects. Only in rare instances would they be beneficial and most adaptations come through recombinations, not SNPs, indels or chromosomal rearrangements.

I assume that you are looking at things from a proportionate point of view, i.e. for every few beneficial mutations there are oodles of deleterious mutations, and therefore there will be far too many deleterious mutations to deal with, is it? I think I will leave that entire issue to gluadys, she's obviously more well-versed in it than I am.

The latest explanation is that neutral and slightly deleterious effects manage to escape natural selection.

Can you quote scientists actually saying this? I can imagine neutral effects escaping natural selection (being purely subject to random drift; although it is hard to make an ironclad case for a mutation being completely neutral) but not deleterious effects.

 

[shernren]

It may help to remember that the only way to pass a mutation from the first carrier to others is via reproduction.

Actually, I don't think the day is too far off when we'll be able to manufacture viruses carrying replacement genes, which can be injected into the bloodstream to modify our genome in situ. But reproduction is the only non-technological way to transmit a mutation.

 

[mark kennedy]

[

A population is a population. It may be a population of paramecia, each of which is a single cell, or a population of beluga whales, each of which is an organism of trillions of cells.

When you are talking about cellular and molecular level evolution population genetics isn't all that helpfull. Bacteria has been a favorite with genetics researchers because they can view the effects over many generations.

The populations of tissue cells in the whales are of no evolutionary interest as they die with the origanism. Only germ line cells carry the whale genome to the next generation.

I really don't know what you are getting at, I am almost sure I said the same thing earlier.

So I don't know what point you are trying to make. Whether we are talking about a unicellular or multi-cellular organism is irrelevant. We are still dealing with a reproductive population

What we are supposed to be talking about is the genetic basis of human evolution. I think we are circling the topic for what reason I do not know.

“They”? Who is “they”? Biologists recognized this decades ago. Perhaps you mean that creationists are finally getting the message that evolutionary produces a bush-like phylogeny rather than a ladder?

Then why do they (whomever you think 'they' are) still put those cartoon transitions that illustrate illusionary lineal descent?

The question of whether evolution selects species in competition as well as organisms within a species is one I haven’t looked into much, but it is probably of less importance than the intra-species competition that leads the species to change. What is importance here is the impact on variants within the human species.

It sure changed a lot I'd say, but I can understand the reluctance to admit the level of divergance. Ape don't turn out to have a common ancestor with humans and it's over for evolution as natural history. The actual science would be unchanged but biologists must be continually reminded that things just look designed. Maybe the reason things don't change at the level that they would have to is that they can't, ever consider that?

No, evolution is about changing the distribution of alleles, not about changing the alleles themselves. Natural selection is the mechanism for changing the distribution of alleles. Your example again shows that you are focusing on individuals. To understand natural selection you must focus on the species as a whole because that is where natural selection is manifested.

I am focusing on the scenerio that covers 5 million years of human evolutionary history. I think that rules out me being focused on Clint mentioned in the paper. The heart of the emphasis is the level of divergance since the last common anceostor we are supposed to have with chimpanzees.

Which is why you have not learned to understand natural selection and continue to make erroneous assumptions about natural selection and evolution.

The only erroneous assumption you ever really take issue one is that the Genesis account is literal reality and it is evolution as natural history is the mythology. 20 nucleotides fixed in the respective genomes per year, 100 per generation or 125Mb over 5 million years is the same ridiculas problem no matter how you slice up the semantics.

I asked first. Are you now admitting that it does not harm the species if less than 5% of the population is afflicted with microcephaly or any other brain disorder you wish to name?

They are rare to begin with, so I would think 5% is about right. The point you seem to be avoiding is no matter the percentage of deleterious effects the benefical one will be dramatically lower.

I will certainly grant that if only 5% of the population carries a beneficial mutation, the species as a whole has not yet benefited.

They tend not to benefit from the bottlenecks that would be nessacary to fix them over time either.

But then we come to the next question. Your “nearly unsolvable” problem is answered when you can answer that.



Again, I asked first. I will deal with your question when you have at least attempted to answer mine.

It's been asked and answered plenty of times. First of all the are so rare there is not earthly way of measuring the rate. Secondly, the are dwarfed by the number of neutral and deleterious effects. I can give you all the diseases and disorders you need but you would be hard pressed to find a beneficial effect from a mutation effecting the human brain. Unless of course Alzeheimers and brain tumors have some selective advantage I am unaware of.

In fact, the answer to both questions is the same. The same process that restricts the spread of deleterious mutations into the population is responsible for making beneficial mutations wide-spread to the point of fixation.

Now you are confusing adaptations with modifications of an existing gene. They are not the same thing, in fact the genes need not be altered signifigantly at all. 200,000,000 nucleotides more in the chimpanzee genome then human but humans have 50 genes chimanzees don't. The differences the account for unique human features are being discovered sure enough. It's getting these changes in the respective genetic codes that has remained elusive to the point of being impossible. At least by any known genetic mechanism and by the way, natural selection is not a genetic mechanism. It's an a priori assumption.

Irrelevant. Natural selection does not care if the mutation it is favoring originated in the current generation or 1,000 generations previously and has now been recombined into a favorable genetic pattern.

Natural selection is not a thinking process, it's a personification. It is considered a force of nature, a pragmatic survival based on the strength of derived characteristics. At a genetic level species are fixed by limits they cannot completly change into another kind. Genes are not as tranposable as we have been led to believe, in fact, most of them are highly conserved.

Obviously. But once selection begins, the number of alleles will be reduced as only the most favorable are transmitted to future generations.

No matter how many times you say that it won't make true. Natural selection is the measurement of amino acid sequences that are changed to the ones that don't (the classic Ka/Ks ratio).

Another bit of vocabulary to get straight. No gene is fixed genome-wide. The relevant concept here is not the genome—which is the total set of coding and non-coding sequences peculiar to the species, but the gene pool—which is the total number of the copies of the genome which exist in the germ line cells of a species’ population. Every gene is just one element in a genome. In each diploid cell, there are two copies of the species genome. In each gamete, there is one copy of the species genome. In the species as a whole there are as many (relevant) copies of the species’ genome as there are germ-line cells. This constitutes the gene pool.

Ok, that sounds like something straight out of a Biology textbook, I see no problem with it. Still, there are a lot of changes at an amino acid sequence level that would have to be altered. This includes gross structural changes like gene duplications still left unaccounted for.

Evolution is a change in the distribution of alleles across the gene pool. Natural selection is the major mechanism for changing this distribution.

Which account for most of the adaptive changes seen in nature quite adequetly unless you insist a single common ancestory of everything.

So let’s go back to that last question. You have agreed that the distribution of deleterious mutations in a population is small. You have (I think) agreed that a species is not unduly harmed by a small proportion of its population being afflicted by such deleterious mutations.

Now, why does the distribution of such deleterious mutations tend to remain restricted to a small part of the population? After all, they seem to have the same opportunity to spread through the population as neutral and beneficial mutations. So why don’t they?


It may help to remember that the only way to pass a mutation from the first carrier to others is via reproduction.

I think the obvious answer is the natural selection eliminates them. That still leaves the central question wide open, how could all those differences have gotten in the respective genomes? We diverge among ourselves by 1/10 of one percent, the divergance level between us and chimanzees is more like 4%. That is just the nucleotide sequence identity with 35 million SNPs, 5 million indel events 90Mb total, and 20 Mb worth of chromosomal rearrangements.

You have an elaborate argument against deleterious and neutral effects being spead through entire populations. Still, I don't see hide nor hair of an explanation for how these sweeping changes occured on such a level.

 

[mark kennedy]

I also know what mitochondria, Golgi apparatus, chloroplasts and the endoplasmic reticulum do, as well as the four levels of protein structure, so I didn't really need that biochemistry primer, but thanks anyway!

I was just trying to point out that we are limited to 64 amino acid sequences. I wasn't sure if you would be able to follow the rest of the discussion if I didn't elaborate a little.

What is happening is that you are assuming that protein modification has to "hit a sweet spot" for evolution to go forward. In one shot evolution has to go from this protein to that protein (both very well defined targets) so in your mind evolution can't do that and therefore it's an inadequate mechanism. But how are you so sure that other proteins won't work?

No real sweet spot here, just a working combination of triplet codons. They have to follow very precise assembly instructions in order to fold into the proper protein. I think most of the changes that alter the changes are accounted for by recombinations, prions turning genes on and off and an abundance of resources as opposed to scarcity. Natural selection is based on competition, adaptation is more the result of mutual benefit and cooperation.

Is there an actual physical principle that forbids natural selection to have synergistic effects, or is this simply a rehashed ID incredulity-of-low-probability argument?

You are limited by the alleles the genes provide. ID is based on irreducible complexity and it is hardly an incredulas argument. It's an ad hominid arguement based on main stream scientific observations of vital systems. Both focus on the sweeping assumptions of Darwinism and naturalistic methodology.

To be frank Mark I don't think you're taking it from the point of view of people living in a land where malaria is endemic. In such places the advantages of having sickle-cell trait outweigh potential energetic costs. Malaria is a killer and anything that slows it down has big benefits.

The sickle-cell trait can cause a slight advantage but modern medicine works a lot better. Malaria is a killer but deformed blood cells are not an adaptation. At the end of the day this is about the postive selection of adaptive traits over time. Ideally, sickle-cell traits would be reduced in favor of improved immunity systems and better treatments for malaria.

[I don't like my terms unquantified - how would you propose to measure "energetic costs"?]

You would need some way of measuring the costs against the benefits. It is really a question of getting the favorable trait working well enough that natural selection preserves it.

I assume that you are looking at things from a proportionate point of view, i.e. for every few beneficial mutations there are oodles of deleterious mutations, and therefore there will be far too many deleterious mutations to deal with, is it? I think I will leave that entire issue to gluadys, she's obviously more well-versed in it than I am.

Mutations don't really provide a lot of great advantages. 98% do nothing at all and most of the rest are deleterious. There are tons of examples of diseases that result from mutations and very few that are of benefit. Personally, I think the question is altogether unanswerable by evolutionary biology.

Can you quote scientists actually saying this? I can imagine neutral effects escaping natural selection (being purely subject to random drift; although it is hard to make an ironclad case for a mutation being completely neutral) but not deleterious effects.

I can dig out the literature when the time comes, right now I am just trying to get back on topic. The spontaneous mutation rate has been measured in all kinds of cells. When the effects are beneficial it is usually a marginal effect over a short period of time.

There is reason to believe that neutral and slightly delerious effects can make contributions over time. Actually, I gave up on making sense of single common ancestory a long time ago. Now I am actually curious about how reading frames can be altered and swapped out. I have seen some anecdotal evidence for this and it has sparked my interest for some time.

Grace and peace,
Mark

 

[shernren]

No real sweet spot here, just a working combination of triplet codons. They have to follow very precise assembly instructions in order to fold into the proper protein. I think most of the changes that alter the changes are accounted for by recombinations, prions turning genes on and off and an abundance of resources as opposed to scarcity.

Rushing for class now, but off the top of my head I'm thinking of flagella evolution:

http://en.wikipedia.org/wiki/Evolution_of_flagella

Regarding the origin of the individual protein components, an interesting paper on the evolution of dyneins[1][2] shows that the more complex protein family of cilial dynein has an obvious ancestor in a simpler cytoplasmic dynein (which itself appears to be a result of a four-fold duplication of a smaller motif). Long-standing suspicions that tubulin was homologous to FtsZ (based on very weak sequence similarity and some behavioral similarities) were confirmed in 1998 by the independent resolution of the 3-dimensional structures of the two proteins.

(emphasis added)

I see minor variations in the "very precise assembly instructions" producing a family of proteins from an ancestral protein here. There aren't really that few possible combinations of working codons, are there?

Natural selection is based on competition, adaptation is more the result of mutual benefit and cooperation.

I don't get what you're trying to say.

You are limited by the alleles the genes provide.

Mutations make new alleles.

ID is based on irreducible complexity and it is hardly an incredulas argument. It's an ad hominid arguement based on main stream scientific observations of vital systems. Both focus on the sweeping assumptions of Darwinism and naturalistic methodology.

I didn't say ID was an incredulous argument I said it was an argument-from-incredulity. And as far as I know ID really has no way to quantify "irreducible complexity" other than assigning a probability to the synergistic parallel evolution of multiple features required in an "irreducibly complex" system, and assuming that a system with a low enough probability must therefore be intelligently designed.

 

[gluadys]

When you are talking about cellular and molecular level evolution population genetics isn't all that helpfull. Bacteria has been a favorite with genetics researchers because they can view the effects over many generations.

It is impossible to talk evolution without talking population genetics even when you are talking about populations of bacteria. It is key to understanding how changes in cells become changes in populations--and that is what evolution is: changes in populations which began as changes in cells.

I really don't know what you are getting at, I am almost sure I said the same thing earlier.

So we are on the same page there. Good.

What we are supposed to be talking about is the genetic basis of human evolution. I think we are circling the topic for what reason I do not know.

The genetic basis of evolution is not limited to the study of mutations and their impact on cells/organisms. It has to include the effect on populations and that means looking at the role of natural selection. You have never displayed any comprehension of how natural selection affects the distribution of mutations. Without that comprehension you have no way to grasp the genetic basis of evolution. Remember evolution is a species-wide process. You have to get above the level of impact on a cell or organism to look at what is happening to those genetic changes on a population basis.

Then why do they (whomever you think 'they' are) still put those cartoon transitions that illustrate illusionary lineal descent?

Who knows, since we don't know who "they" are. I think I can be confident that those cartoons are not being published in scientific research papers.

It sure changed a lot I'd say, but I can understand the reluctance to admit the level of divergance.

Well, in this case we are not looking at competition of one species with another, since chimps and humans have not been competing with each other directly (unless you count the current impact of human activity on chimp habitat which is reducing the population of chimps.)

So let's get back to what process was happening to change humans and human ancestors over the last 5 million years. The key here is to understand the process of change and divergence first. Then you have a basis for commenting on the amount of divergence. Right now, you claim the level of divergence is impossible, but you have nothing but your own incredulity as evidence for that claim.

If you learn the process of divergence, you may be able to put some teeth in your argument.

The heart of the emphasis is the level of divergance since the last common anceostor we are supposed to have with chimpanzees.

The process applies to all situations of divergence, not just this one. But it does apply to this one too. Now, just to check. Are you clear on the difference between changing alleles and changing the distribution of alleles? What does the latter phrase mean to you?


Next question: how is the distribution of a pair of alleles changed?

20 nucleotides fixed in the respective genomes per year, 100 per generation or 125Mb over 5 million years is the same ridiculas problem no matter how you slice up the semantics.

What is the relationship between the distribution of an allele in the gene pool and the fixation of that allele in the genome?

btw, it is permissible to answer "I don't know". I just want to avoid going over what you already know. But if the question mystifies you, I will explain.

They are rare to begin with, so I would think 5% is about right.

In what sense do you mean "rare"? I think you are going off on a tangent here.

5% of what is about right?

The point you seem to be avoiding is no matter the percentage of deleterious effects the benefical one will be dramatically lower.

This is what makes me think you are going off on a tangent. Do you not realize that if a mutation with a deleterious impact affects 5% of a population, then the beneficial impact of not having that mutation affects 95% of the population. The beneficial impact is dramatically higher, not lower.

They tend not to benefit from the bottlenecks that would be nessacary to fix them over time either.

Bottlenecks are not necessarily required. I grant that fixation is likely to occur more rapidly in a small population, but as long as there is a benefit to having a new variable, it will eventually fixate even in a larger population.

It's been asked and answered plenty of times. First of all the are so rare there is not earthly way of measuring the rate. Secondly, the are dwarfed by the number of neutral and deleterious effects. I can give you all the diseases and disorders you need but you would be hard pressed to find a beneficial effect from a mutation effecting the human brain. Unless of course Alzeheimers and brain tumors have some selective advantage I am unaware of.

Its been asked, but not answered. Or rather, every time it has been asked, your answer has been irrelevant to the question. You go off onto the same tangent as you do here talking about the deleterious impact of harmful mutations on the individuals who carry them. You totally lose focus of the fact that evolution happens to species, not individual cells or organisms.

You say "there is not earthly way of measuring the rate" but you don't say which rate you are speaking of. Is it the rate of mutations per cell replication? Is it the ratio of harmful/beneficial mutations per 1 million mutations? Is it the ratio of harmful to beneficial mutations that affect a cell or organism? Or is it the rate at which a particular harmful mutation shows up in a species?

Only the last is pertinent to evolution.

Now you are confusing adaptations with modifications of an existing gene.

I am not confusing anything. In the first place, all mutations are modifications of existing genes. Not every genetic modification, however, is expressed as a modification of the organism that carries it.

When the genetic modification (aka mutation) is expressed as a cellular or organic modification, it is called a variation. If the variation increases the fitness level of the organism, it is an adaptation.

It's getting these changes in the respective genetic codes that has remained elusive to the point of being impossible.

I've got news for you. Have you ever heard of reproduction? Really, Mark, how did you think changes in genetic codes are spread?

At least by any known genetic mechanism and by the way, natural selection is not a genetic mechanism.

Do you remember reminding me that cells as well as multicellular organisms are populations? Well genes are populations too. They also replicate and they compete with each other to replicate more of themselves. And natural selection affects the outcome of that competition too. So it is a genetic mechanism. And if the effect of natural selection is directly on cells or organisms, it is still also indirectly on genes. So how can it not be a genetic mechanism.

Natural selection is not a thinking process, it's a personification.

You are right, it is not a thinking process, and when it is spoken of anthropomorphically, as it often is, it is a personification.

It is considered a force of nature

Those who think of natural selection in this way do not understand it. It is not a force. It is more like an algorithm. The force involved is environmental pressure aka selective pressure. But that force is highly variable and may even be absent. Nothing decrees that a species must evolve in the absence of environmental pressure. And since evolution also depends on the presence or new occurrence of variation (which in turn depends on genetic change) it is possible that no adaptive evolution will occur even in the face of environmental pressure.

a pragmatic survival based on the strength of derived characteristics.

Could you clarify what you mean by this?

At a genetic level species are fixed by limits they cannot completly change into another kind.

And the theory of evolution does not predict a complete change into another kind.

Genes are not as tranposable as we have been led to believe, in fact, most of them are highly conserved.

What study backs up this statement?

No matter how many times you say that it won't make true.

No wonder you think fixation is impossible. This is the meaning of fixation---the elimination of alternative alleles in favour of the most adaptive one, which becomes the species norm. Early tetrapods had six, seven or eight digits, but those alternatives were eliminated in favour of the pentadactyl limb, which humans still retain as the species norm.

Natural selection is the measurement of amino acid sequences that are changed to the ones that don't (the classic Ka/Ks ratio).

You have it backwards. The Ka/Ks ratio is a measure of natural selection. When it is greater than 1, it is an indication of adaptive selection and therefore of a beneficial mutation.

Ok, that sounds like something straight out of a Biology textbook, I see no problem with it. Still, there are a lot of changes at an amino acid sequence level that would have to be altered. This includes gross structural changes like gene duplications still left unaccounted for.

I should hope it does. But apparently you did not understand it.

Try this. Changes at an amino acid sequence level occur one gene at a time. Gross structural changes like gene duplications occur in one chromosome at a time.

Both occur in one cell at a time.

Evolution occurs when these changes spread to other cells or organisms in the population.

Natural selection is what governs the distribution of these changes from the single gene or chromosome in which they first occurred to the genes and chromosomes in other cells and organisms.

So let's start with a simple question. In bacterial cell #9277 out of a population of 500 million cells, an amino acid sequence is changed. How is that change spread to two cells?

Which account for most of the adaptive changes seen in nature quite adequetly unless you insist a single common ancestory of everything.

How does natural selection account for these adaptive changes adequately without a common ancestor? How is that possible?

I think the obvious answer is the natural selection eliminates them.

OK, you have named the process. Now describe it. How does natural selection eliminate deleterious mutations from a population (or as is more usual, keep them restricted to a small proportion of the population.)


Again, may I note that it is ok to answer "I don't know".

That still leaves the central question wide open, how could all those differences have gotten in the respective genomes?

One gene in one cell at a time. Of course, since the population consists of many cells/organisms, you can have many changes happening simultaneously, but each one begins in one particular gene in one particular cell in one particular organism.

I don't know why you have a problem with this.

You have an elaborate argument against deleterious and neutral effects being spead through entire populations. Still, I don't see hide nor hair of an explanation for how these sweeping changes occured on such a level.

And you have an elaborate argument against beneficial effects being spread through entire populations. Actually, in both cases, its not elaborate at all. Natural selection is the essence of simplicity.