Pete's Quite Thread post

[mark kennedy]

To start, estimates on beneficial mutation rates are almost non-existent.

That is because beneficial mutations are virtually nonexistant and you want them to be fixed, in every generation, for how many generations? By the way, you are looking at about a 1 1/2 million year period in which most of the mophological changes that started with Homo rudolfensis and Homo habilis about 2 1/2 a million years ago to the emergance of Homo sapiens about 1/2 a million years ago. At best we are looking at a 2 1/2 million year period since the skulls of the two original Homo species were not much bigger then that of a chimp. I have tried to explain this to you but for whatever reason you just don't get it. Follow the white rabbit Neo.

http://www.mnh.si.edu/anthro/humanorigins/ha/a_tree.html


"Their low frequency, however, has made this class of mutations almost inaccessible for systematic studies. In the absence of experimental data, the distribution of the fitness effects of beneficial mutations was assumed to resemble that of deleterious mutations." (Fitness effects of advantageous mutations in evolving Escherichia coli populations)

Beneficial effects of the fitness of what exactly, you do know that most of the mutations will be neutral right? Also that most of the outgroups will be evolutionary dead ends. First lets consider the exponential

"From this data set, we estimate the rate of beneficial mutations to be 4 × 10^−9 per cell and generation. Consistent with an exponential distribution of the fitness effects, we observed a large fraction of advantageous mutations with a small effect and only few with large effect."

There is a large fraction with a small effect and a few with a large effect. This leaves us with a mean selection coefficient for beneficial effects of 0.02. They go on to say that beneficial mutations are rare and they cite three earlier research projects that had the same problem. What makes this harder is that a large fraction of these mutations are deleterious and most of them are purged. Again they cite other studies that reached this conclusion. They proposed an experimental marker system that, in theory at least, could track the beneficial mutations. This is to find the limits for the fixation of beneficial mutations they called the 'Malthusian fitness parameter'. You might recall that Darwin's natural selection was based on the geometric growth of populations. This is Darwin under the microscope Pete:

"In October 1838, that is, fifteen months after I had begun my systematic inquiry, I happened to read for amusement Malthus on Population, and being well prepared to appreciate the struggle for existence which everywhere goes on from long- continued observation of the habits of animals and plants, it at once struck me that under these circumstances favourable variations would tend to be preserved, and unfavourable ones to be destroyed. The results of this would be the formation of a new species. Here, then I had at last got a theory by which to work".(Charles Darwin, from his autobiography. (1876))

What you have failed to take into consideration, as I have told you repeatedly, are the neutral and deleterious effects on populations. Bear in mind that Hominids have a high deleterious mutation rate:

"Under conservative assumptions, we estimate that an average of 4.2 amino-acid-altering mutations per diploid per generation have occurred in the human lineage since humans separated from chimpanzees. Of these mutations, we estimate that at least 38% have been eliminated by natural selection, indicating that there have been more than 1.6 new deleterious mutations per diploid genome per generation. Thus, the deleterious mutation rate specific to protein-coding sequences alone is close to the upper limit tolerable by a species such as humans that has a low reproductive rate"


High genomic deleterious mutation rates in hominids.

"Our data suggest that indels within coding regions represent one of the major mechanisms generating protein diversity and shaping higher primate species."​

What is more, you didn't seem to realize just how many indels would have had to be fixed in the protein coding sequences:

"Thirty-two genes show changes modifying either the first ATG or the stop codon in at least one of their associated transcripts."​

The study revealed only 39 genes that were identical, out of 231 examined. Do you really expect me to believe that this is not a problem with evolutionary theory?

"39 genes show an identical amino acid sequence between human and chimpanzee, including seven in which the nucleotide sequence of the coding region is also identical."

"Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins). In addition, 87 genes in the catalogue show mutations in at least one of the splice sites."​

DNA sequence and comparative analysis of chimpanzee chromosome 22

Speaking of proteins:

"The chimpanzee is our closest living relative. The morphological differences between the two species are so large that there is no problem in distinguishing between them. However, the nucleotide difference between the two species is surprisingly small. The early genome comparison by DNA hybridization techniques suggested a nucleotide difference of 1–2%. Recently, direct nucleotide sequencing confirmed this estimate. These findings generated the common belief that the human is extremely close to the chimpanzee at the genetic level. However, if one looks at proteins, which are mainly responsible for phenotypic differences, the picture is quite different, and about 80% of proteins are different between the two species."

Eighty percent of proteins are different between humans and chimpanzees

Mutation rates are no problem for evolution? Come on Pete, get real.

 

[Split Rock]

However, if one looks at proteins, which are mainly responsible for phenotypic differences, the picture is quite different, and about 80% of proteins are different between the two species."

Eighty percent of proteins are different between humans and chimpanzees

Mutation rates are no problem for evolution? Come on Pete, get real.

From the above paper (Table 3) : Of the 127 protein-coding human genes studied,
1. 25 are identical to chimp genes
2. 11 are identical to gorilla genes
3. 7 are identical to orangutan genes
4. 4 are identical to gibbon genes

Do you see a pattern here? I sure do.

Also, can you explain why there is more identical genes between chimps and humans than between chimps and gorillas?

 

[mark kennedy]

From the above paper (Table 3) : Of the 127 protein-coding human genes studied,
1. 25 are identical to chimp genes
2. 11 are identical to gorilla genes
3. 7 are identical to orangutan genes
4. 4 are identical to gibbon genes

Do you see a pattern here? I sure do.

Well, if parsimony is your only consideration then I suppose you have something there. I don't know how you think this gives us for genetic basis for major morphological changes but, yea, there would seem to be a pattern. Still, homology does not gives us any way of testing the assumption of single common ancestory, much less the effect of the mutation rate on adaptation.

Also, can you explain why there is more identical genes between chimps and humans than between chimps and gorillas?

Nope, can you explain how 83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level?

 

[mikeynov]

Holy **** - how can Mark keep re-making what is the same fundamental post over and over? Particularly after there's been more than adequate replies to every single one of his points.

Mark, if you want a more in-depth discussion of population genetics, my recommendation would be to take this discussion here or here.

 

[Pete Harcoff]

That is because beneficial mutations are virtually nonexistant and you want them to be fixed, in every generation, for how many generations?

Where did I say they had to be fixed in every generation? Please show me.

By the way, you are looking at about a 1 1/2 million year period in which most of the mophological changes that started with Homo rudolfensis and Homo habilis about 2 1/2 a million years ago to the emergance of Homo sapiens about 1/2 a million years ago. At best we are looking at a 2 1/2 million year period since the skulls of the two original Homo species were not much bigger then that of a chimp. I have tried to explain this to you but for whatever reason you just don't get it. Follow the white rabbit Neo.

Except that rates of morphological changes and genetic changes are not necessarily analogous. Without knowing the exact changes required for certain morphological features, it's premature to suggest that a greater level of genetic change was required for specific time period.

Beneficial effects of the fitness of what exactly, you do know that most of the mutations will be neutral right?

I'm not talking about most mutations. I'm talking about a very restricted subset. We've argued this before and you just don't get it.

What you have failed to take into consideration, as I have told you repeatedly, are the neutral and deleterious effects on populations.

And you have never told me why this is a problem.

Mutation rates are no problem for evolution? Come on Pete, get real.

All I did was take some numbers and crunch them. You continue to harp on the differences between chimps and humans as though you've stumbled onto some magical secret that no one else knows. Yes, there are differences between humans and chimps. So what? I'm merely looking at available data on mutation rates. Do you have a problem with the data? Yes, no?

 

[Pete Harcoff]

Holy **** - how can Mark keep re-making what is the same fundamental post over and over? Particularly after there's been more than adequate replies to every single one of his points.

Because mark is talking apples while everyone else is talking oranges.

My argument is this: based on the limited data available, mutation rates aren't a problem.

Mark's argument is this: we don't know all the specifics of how humans evolved, therefore it didn't happen.

Those are two different lines of argument.

 

[mikeynov]

I'd also like to point out that, to date, Mark still doesn't seem to understand the concepts of positive and negative selection. In Mark-land, as far as I can tell, all mutations would propagate throughout a population at the same frequency - since most are neutral, most would have no effect, but since so few are beneficial, they'd be drowned out by all the other ****.

But that's what he doesn't seem to understand - mutations are defined by their impact on reproductive success in terms of beneficial, neutral, or deleterious. Positive selection acts to increase the frequency of these mutations within some population over time whereas negative selection acts to weed out the deleterious mutations. Mark doesn't seem to believe this happens.

 

[Pete Harcoff]

But that's what he doesn't seem to understand - mutations are defined by their impact on reproductive success in terms of beneficial, neutral, or deleterious. Positive selection acts to increase the frequency of these mutations within some population over time whereas negative selection acts to weed out the deleterious mutations. Mark doesn't seem to believe this happens.

I don't think mark believes in natural selection.

I'm actually tempted to write a computer simulation based on some of this data to see the actual effect. I've got some Comp Sci courses coming up, so maybe I'll write a program for extra practice.

 

[mikeynov]

I don't think mark believes in natural selection.

I'm actually tempted to write a computer simulation based on some of this data to see the actual effect. I've got some Comp Sci courses coming up, so maybe I'll write a program for extra practice.

If you write that, you should post it here. Of course, creationists would cry conspiracy (that you fixed the results).

But yah, if Mark doesn't buy into natural selection (which isn't very hard to understand), I'm not sure if it's worth replying to his one-post-rephrased-in-different-ways-and-supposed-to-somehow-be-a-revelation-over-and-over-again anymore.

 

[mikeynov]

Also, as a thought, Mark, you could enroll in a population genetics course at a local university, ya know. You seem into it, so I'd say go for it.

 

[mark kennedy]

Ok, the protein coding genes are unimportant because there is no mention of them in your posts. Pete's post gives the transition from ape to human a 5 million year space of time for his 'number crunching' and it does not follow natural history as evolutionists describe it. Now if you want to apply the beneficial mutation rate to human evolution it has to apply to something tangable, at some point, like the protein coding genes.

How long are you guys going to take to get the obvious. Mutations are transcript errors that result in disease and disorders like cancer and Fragil X syndrome, not an explosion in the size, density and complexity of the human brain.

You don't like me harping on this point, I'll tell you how to shut me up once and for all. Show me one benefical mutation that has been directly observed or demonstrated in modern science effecting the human brain. The list of deleterious effects is as long as your arm, where are all of these beneficial mutations that natural selection is supposed to be preserving?

 

[Pete Harcoff]

Ok, the protein coding genes are unimportant because there is no mention of them in your posts. Pete's post gives the transition from ape to human a 5 million year space of time for his 'number crunching' and it does not follow natural history as evolutionists describe it.

You're right. I could probably allow for a greater length of time. But I was being generous.

Now if you want to apply the beneficial mutation rate to human evolution it has to apply to something tangable, at some point, like the protein coding genes.

So? Like I said, I'm already working with a subset of mutations, not all mutations.

How long are you guys going to take to get the obvious. Mutations are transcript errors that result in disease and disorders like cancer and Fragil X syndrome, not an explosion in the size, density and complexity of the human brain.

See, this is the problem. You have the typical "all mutations are bad" creationist thought process going on. You need to step outside your box and realize that all mutations aren't bad.

You don't like me harping on this point, I'll tell you how to shut me up once and for all. Show me one benefical mutation that has been directly observed or demonstrated in modern science effecting the human brain. The list of deleterious effects is as long as your arm, where are all of these beneficial mutations that natural selection is supposed to be preserving?

I've already explained to you the logistics of this and why such a mutation would be extremely difficult to find. You'll just have to be patient.

In the mean time, people have given you examples of other beneficial mutations (including in the human species), but you systematically ignore or reject them.

 

[mark kennedy]

You're right. I could probably allow for a greater length of time. But I was being generous.

That is not tied to anything of substance, the crucial transition started about 2 1/2 million years ago and there is not a shred of evidence to the contrary.

"As the fossil record began to expand and more early human fossils were found dating to the period between 2 million and 1 million years ago, some questions as to the validity of this hypothesis were raised...ER 1470 has a cranial capacity of 775cc, where ER 1813 has a cranial capacity of only 510cc (which is above the australopith average, but well below the accepted 600cc cutoff for Homo) "

http://www.mnh.si.edu/anthro/humanorigins/ha/habdebate.html

So tell me Pete, what is the cranial capacity of modern humans and how does it relate to the mutation rates you played with?

So? Like I said, I'm already working with a subset of mutations, not all mutations.

So, you failed to factor in neutral and harmfull effects. You were just assuming there were as many beneficial effects as there were harmfull even thought there is no real evidence that they are.

See, this is the problem. You have the typical "all mutations are bad" creationist thought process going on. You need to step outside your box and realize that all mutations aren't bad.

Not all bad, if you can discern the difference between a transcript error and an alternative reading frame, transpostion...et al.

I've already explained to you the logistics of this and why such a mutation would be extremely difficult to find. You'll just have to be patient.

Yea, benefical effects from a mutation would be hard to find, harmfull ones are not. So much for you base assumption.

In the mean time, people have given you examples of other beneficial mutations (including in the human species), but you systematically ignore or reject them.

That's right, resistance to AIDs is a defective receptor and the nylon bug is an alternative reading frame. That is the extent to which you have addressed the identification of benefical effects from mutations.

 

[Pete Harcoff]

That is not tied to anything of substance, the crucial transition started about 2 1/2 million years ago and there is not a shred of evidence to the contrary.

<snippage>

So tell me Pete, what is the cranial capacity of modern humans and how does it relate to the mutation rates you played with?

Except that we're dealing with divergence between to species as a whole. We have no genetic benchmark from 2.5 million years ago.

So, you failed to factor in neutral and harmfull effects. You were just assuming there were as many beneficial effects as there were harmfull even thought there is no real evidence that they are.

No, I was assuming there are way fewer beneficial mutations than neutral or deleterious ones.

Not all bad, if you can discern the difference between a transcript error and an alternative reading frame, transpostion...et al.

And?

Yea, benefical effects from a mutation would be hard to find, harmfull ones are not. So much for you base assumption.

What base assumption? I never assumed that beneficial mutations are on greater or even equal terms compared to harmful mutations. Did you even bother to read my post?

That's right, resistance to AIDs is a defective receptor and the nylon bug is an alternative reading frame. That is the extent to which you have addressed the identification of benefical effects from mutations.

Actually, there were plenty more examples given. You just proved me right, you are selectively ignoring or discarding what you don't like.

 

[mark kennedy]

Except that we're dealing with divergence between to species as a whole. We have no genetic benchmark from 2.5 million years ago.

We have the cranial capacity but I am not supprised that you failed to realize this.

No, I was assuming there are way fewer beneficial mutations than neutral or deleterious ones.

No need to assume, it has been directly observed and demonstrated.

And?

And, you should learn the difference.

What base assumption? I never assumed that beneficial mutations are on greater or even equal terms compared to harmful mutations. Did you even bother to read my post?

I read your post, did you read your source material?

"The central role of beneficial mutations for adaptive processes in natural populations is well established. Thus, there has been a long-standing interest to study the nature of beneficial mutations. Their low frequency, however, has made this class of mutations almost inaccessible for systematic studies. In the absence of experimental data, the distribution of the fitness effects of beneficial mutations was assumed to resemble that of deleterious mutations."

Assumed to resemble? Give me a break, there is no basis for comparison.

Actually, there were plenty more examples given. You just proved me right, you are selectively ignoring or discarding what you don't like.

Examples of beneficial mutations that effect the human brain, neural systems or other vital organs. Get with the program, we are talking about the differences you alluded to in your Quite Thread post, you even cited and linked the Chimpanzee Chromosome Consortiums paper so you should at least address the findings of their research.

 

[mikeynov]

We have the cranial capacity but I am not supprised that you failed to realize this.

He said genetic benchmark. Morphology can shed some light as to genetic divergence, but you can't compare genomic sequences between humans and stuff that hasn't been around a couple million years. P.S. Don't you deny an old earth time scenario in general?

No need to assume, it has been directly observed and demonstrated.

If it's been demonstrated that beneficial mutations are less frequent than deleterious mutations, this implies we have some figures to work with for their prevalence. Pete cited one example in his thread, which seemed a very conservative estimate - what are you working off of?

 

[LordoftheScythe]

Mark, are you wanting to be shown a beneficial mutation of the brain?? How would we observe that? I'm not even sure that we know what a "normal" brain looks(works) like. Wouldn't we have to look at a huge number of brains to first figure out what a normal one is like(works) and then look for changes in years to come? The human brain is not the same in everyone and there is a vast range of intelligence. Are you assuming that this range of intelligence that we observe isn't the product of mutations? If it isn't, then how would we know what a mutation of the brain is?

A problem I see with these observable changes is that waaay back there were more niches left to fill. How about the first creature to walk/slither on land? They had so much they could become compared to their ancestors.

Humans aren't exactly struggling to survive, so the beneficial mutations aren't even really showing themselves and spreading through the population. What mutation could someone have that was so good that they survived better than others and had more children? And how long would that mutation take to increase its frequency in the population? Do people that are smarter have more children? Not really. Do people who are stronger have more children? Not really. Greater bone density? Not really. Increased disease resistance? Maybe, but we have cures and such.

How quickly a mutations frequency increases is based on the differential reproductive success and the size of the population. Can you think of any mutation that would be good enough. You can bet that anything essential, way back, spread quickly and is now considered normal.

 

[mikeynov]

Mark, are you wanting to be shown a beneficial mutation of the brain?? How would we observe that? I'm not even sure that we know what a "normal" brain looks(works) like. Wouldn't we have to look at a huge number of brains to first figure out what a normal one is like(works) and then look for changes in years to come? The human brain is not the same in everyone and there is a vast range of intelligence. Are you assuming that this range of intelligence that we observe isn't the product of mutations? If it isn't, then how would we know what a mutation of the brain is?

A problem I see with these observable changes is that waaay back there were more niches left to fill. How about the first creature to walk/slither on land? They had so much they could become compared to their ancestors.

Humans aren't exactly struggling to survive, so the beneficial mutations aren't even really showing themselves and spreading through the population. What mutation could someone have that was so good that they survived better than others and had more children? And how long would that mutation take to increase its frequency in the population? Do people that are smarter have more children? Not really. Do people who are stronger have more children? Not really. Greater bone density? Not really. Increased disease resistance? Maybe, but we have cures and such.

How quickly a mutations frequency increases is based on the differential reproductive success and the size of the population. Can you think of any mutation that would be good enough. You can bet that anything essential, way back, spread quickly and is now considered normal.

The problem is that Mark still doesn't know what a beneficial mutation is. To Mark, a beneficial mutation would grant us telepathy or laservision - he still doesn't "get" that beneficial is always contextual to environmental demands.

If there are no selective pressures on increased cognitive/brain capacity in a human population, there would be nothing driving an increase in frequency of mutations which accomodate this. And Mark never coughed up a way to know who we'd test in the first place, and probably never will.

See, to creationists like Mark, gaps in knowledge = opportunities to strike. Mark literally ignores all the evidence for common ancestry we do have, and demands that we show him the step-wise process, mechanistically, of how divergence between man and his closest extant relatives occurred. Failure to do so "proves" in Mark's mind that it's all a big lie.

Note: this is why nobody in the field takes creationists seriously, and why the perception of said individuals is that they're nothing but naysayers. Because, by and large, they are.

 

[notto]

Has this been discussed in these 'brain' talks?

http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0020134

just curious.

Thoughts?

 

[mark kennedy]

Look, the topic of discussion is the mutation rate and how it accounts for uniquely human traits. There was not that much source material covered but for whatever reason you guys missed it. That's ok, you are evolutionist and that is allowed. But don't let that confuse you with the ability to defend a refuted point, namely, mutation rates and the evolution of the human brain.

You might try acutally reading the post in question.