Pete's Quite Thread post

[jnhofzinser]

on what basis do you make that claim?

It may be said that

natural selection is daily and hourly scrutinising, throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good;

The point being that natural selection need not (in fact, does not) select for positive traits; rather, it selects against the alternatives.

 

[Jet Black]

The point being that natural selection need not (in fact, does not) select for positive traits; rather, it selects against the alternatives.

"preserving and adding up all that is good"

or can you not read?

Natural selection, in it's most simple description, is nothing more than differential reproductive success - those organisms with genotypes that result in them producing more than the average number of offspring for their gene pool will see those genes spread at the expense of others. there is no real "selection" taking place. claiming that there is "selection for or against" is a bit silly really.

and on top of that, your argument is horribly weak. I could just as easily say that natural selection selects all the positives by ensuring they have more offspring in the next generation. this is ultimately why I prefer the description of differential reproductive success. it results in less silly arguments like yours.

 

[jnhofzinser]

your argument is horribly weak.

What argument is that? We were talking about rates of beneficial mutations.

"or can you not read?"

(if you insist upon reading nonsense into things I've written here, let's take it up elsewhere, and not divert a thread that, at least up until recently, was remarkably focussed)

 

[gluadys]

The point being that natural selection need not (in fact, does not) select for positive traits; rather, it selects against the alternatives.

That's just playing with words. Every time something is selected for, something else is selected against. But the reverse works as well. Every time something is selected against, something else is selected for. So one could just as well say that all natural selection is positive.

 

[Jet Black]

What argument is that? We were talking about rates of beneficial mutations.

you were claiming things are not selected for, and claiming that they were only selected against. I was showing you your argument was nonsense.

"or can you not read?"

go go gadget change arguments mid flow.

(if you insist upon reading nonsense into things I've written here, let's take it up elsewhere, and not divert a thread that, at least up until recently, was remarkably focussed)

If you don't want your nonsense exposing, just don't type it in

 

[Tomk80]

You also said quite clearly that you thought 64k was sufficient.

No, he did not make any statements on whether that was sufficient or not. He stated that this was a lower estimate and that this was would he would use for his model. Whether it was enough or wasn't, was not relevant to the subject he presented.

You are correct. Let me amend: the evidence is clear that the rate of "alleles appearing and being fixed in a population" (i.e., the sense in which we were discussing evolution) in the last 2000 years (with ~279k BMs) is not even remotely approaching the rate being claimed for the last 5M years (with ~64k BMs)

And how do you measure this? Again, what is a beneficial mutation?

In Pete Harcoff's post in the quiet thread, a beneficial mutation is any mutation that gives even a slight benefit. Estimates of this have not been made in humans, because we have no idea how to do that (since we have not yet mapped all alleles present in the total human population, nor have we mapped the precise function of all alleles in the complete human population, we have no way of doing so). Pete used a conservative estimate based on beneficial mutation rates in bacteria, which some of the only data available.

Yes. This is in keeping with the "fixation factor" the arithmetic needs. However, as a first approximation, the "fixation" is simply a matter of time. This would suggest the remarkable (and almost certainly erroneous) conclusion that THE ALLELES NECESSARY FOR A NOTICEABLE LEAP IN HUMAN EVOLUTION ARE ALREADY PRESENT IN THE POPULATION. Since you cannot possibly be supporting this conclusion, can you improve upon the "fixation" approximation so that this embarrassing issue does not arise?

Nowhere did Pete state that, and nowhere does this follow from what Pete stated.

Now it is my turn to accuse you of a "gross misunderstanding of evolution": selective pressure is always negative. If alleles supporting "dramatic leaps in human intellect" were present in the population, there is no reason to think that they would not eventually become fixed.

Selective pressure is not always negative. Whether it is negative or positive depends on the creature you are looking at. One could just as well argue that selective pressure is always positive (since it always favors the organisms that have more offspring).

 

[jnhofzinser]

My apologies for permitting the thread to be sidetracked.

The point being addressed was:

I don't think you're going to see dramatic leaps in human intellect or anything, because there's no selective pressure on it.

The response that I was trying to make was:

"selective pressure" is not necessary for the fixation of "dramatic leaps in human intellect"

If anyone really, really wants to fight the "selection for/against" battle, I suggest they take it up with Jeff:

natural selection does not select for positive characteristics, is selects against negative characteristics.

On the other hand, if you would like to explain why the roughly 279,000 beneficial mutations introduced into human genetics over the last 2000 years have not resulted (will not result?) in any noticeable difference in human-kind, I'm all ears.

 

[jnhofzinser]

Whether it was enough or wasn't, was not relevant to the subject he presented

Surely you jest: in the context of Pete's Quiet Thread post, 64k BMs represented sufficient support for the difference between the chimp/human-common-ancestor and human-kind. Do you not agree?

...nowhere does this follow from what Pete stated

It most certainly does. Read more carefully. (Off to work -- will check back later)

 

[Tomk80]

My apologies for permitting the thread to be sidetracked.

I don't think you're going to see dramatic leaps in human intellect or anything, because there's no selective pressure on it.

The point being addressed was:
[/i]The response that I was trying to make was:

"selective pressure" is not necessary for the fixation of "dramatic leaps in human intellect"

So what do you think is necessary for the fixation of dramatic leaps in human intellect if it isn't selective pressure?

If anyone really, really wants to fight the "selection for/against" battle, I suggest they take it up with Jeff:

I'd be happy to take it up with Jeff. I would argue that Natural selection does both. That's why I'm getting increasingly less happy with the term natural selection, and would go with differential reproductive succes (as Jet Black suggests), because that term describes much more specifically what natural selection does.

In fact, I'd suggest natural selection does both (select for and against). It both selects for mutations that cause creatures to get more offspring as it selects against mutations that cause creatures to get less offspring.

On the other hand, if you would like to explain why the roughly 279,000 beneficial mutations introduced into human genetics over the last 2000 years have not resulted (will not result?) in any noticeable difference in human-kind, I'm all ears.

Could you first define what you understand under a beneficial mutation, and why these mutations would have to have resulted in noticeable differences according to you.

 

[Tomk80]

Surely you jest: in the context of Pete's Quiet Thread post, 64k BMs represented sufficient support for the difference between the chimp/human-common-ancestor and human-kind. Do you not agree?

Yes, but nowhere in his post did he present this as a set in stone statement. It is a lower limit estimate he used. He did not go into it's validity, nor was the purpose of his post to discuss it's validity.

It most certainly does.

Read more carefully. (Off to work -- will check back later)

No it doesn't. The alleles could have arisen during that time and then be fixed. Nowhere does it follow from Pete's statement that the alleles that became fixated had to be present in the population from the beginning.

 

[Tomk80]

As a quick sidenote, the link you provided linked to the wrong page. I think you ment to link to here: http://bearcastle.com/blog/?p=184. I agree with the response given by RPM on that page.

 

[Pete Harcoff]

You also said quite clearly that you thought 64k was sufficient.

Indeed. Based on estimates of differences between humans and chimps, I think it would take at least a coupld hundred thousand mutations in protein coding DNA. Of which, a chunk would be beneficial. But I don't know how many, so don't claim I think it's necessarily 64k.

Yes. This is in keeping with the "fixation factor" the arithmetic needs. However, as a first approximation, the "fixation" is simply a matter of time. This would suggest the remarkable (and almost certainly erroneous) conclusion that THE ALLELES NECESSARY FOR A NOTICEABLE LEAP IN HUMAN EVOLUTION ARE ALREADY PRESENT IN THE POPULATION. Since you cannot possibly be supporting this conclusion, can you improve upon the "fixation" approximation so that this embarrassing issue does not arise?

But they have to accumulate. Say it takes 50k beneficial mutations to go from a common ancestor to a human. Even if all 50k are present in the population, that doesn't matter. They'd need accumulate until they are present in every individual.

And btw, based on general mutation rates in humans, there is mathematically enough variation to rewrite the human genome several times over. BUT, all that variation is not concentrated in a single individual. Rather, it's spread out through the entire population.

Now it is my turn to accuse you of a "gross misunderstanding of evolution": selective pressure is always negative. If alleles supporting "dramatic leaps in human intellect" were present in the population, there is no reason to think that they would not eventually become fixed.

Sure there is. Stupid people still breed. It's not a selective factor.

 

[jnhofzinser]

But they have to accumulate.... [variation] is spread through the entire population

I understand. So are you suggesting that there IS sufficient genetic variation in the CURRENT human population to create a new species? (The distribution of variation suggests some fascinating research venues or conjectures -- suppose, for example, we were to be able to map the distribution of two related species A & B, and then breed the (viable) A* that was genetically "closest" to a B, and the (viable) B* that was genetically "closest" to an A -- I wonder how similar/different A* and B* would be).

[Intelligence is] not a selective factor.

It is clear that I have not been at all clear

The point that I was so unsuccessful in trying to make is that the mechanisms of evolution, while appropriate to prehistoric humanity, are not exactly appropriate to historic humanity. In fact, one could argue that an allele arising in the population, unless specifically reducing the chance of reproduction, is almost certain to survive (given our cultural all-but-elimination of natural selection). Moreover, if the effect of any such allele was cultural "success", one would expect it to thrive. The convergence of successful alleles in a single individual is then (as a first approximation) simply a matter of time.

 

[mark kennedy]

The implications of the mutation rate of the functional genome in bacteria being extended to hominid mutation rates left out two important factors.

1. The effects of deleterious mutations ranging from cell death to degenerative disease effecting overall populations.

This was never factored in even though this is the most common effect observed in phenotypes. The mutation must get through the cell cycle checkpoints, then get fixed in the genome and ultimatly create a new allele the creates a beneficial effect.

This doesn't take into account fixation of neutral or even possibly deleterious mutations which could account for many more differences between humans and chimps.

2. The homology of chimpanzee and human genomes is grossly over estimated.

So what does that mean? Well, the estimated difference between human and chimp genomes is typically less than 2% (though one study put the difference between critical genes at only 0.6%).

At best the overall estimates are 95% (see Divergence between samples of chimpanzee and human DNA sequences is 5%, counting indels ) taking into account the indels Pete was well aware of. What is more over 20% of the protein coding sequences show gross structural changes, another fact Pete was well aware of. I know this because he pressed me to find in the chimpanzee chromosome 22/human chromosome 21 paper to show him where the functional part of the genome was effected, I found this:

"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.(see protein coding characterization in, Nature 429, 382 - 388 (27 May 2004) cited and linked in the Quite Post Thread)

The benefical mutation rate for hominids has been estimated for decades and evolutionists are desperatly trying to hide the fact that it is ridiculasly high to be the result of random mutations. I have deliberatly avoided creationist literature but I see no reason to continue quoting solely from secular sources since they are saying the exact same thing.

"Using many long-range human PCR primers (primers used to sequence 10,000 bases at a time) that spanned 32.4 Mb (1Mb = 1 million bases) of human chromosome 21, approximately 27 Mb of chimpanzee chromosome 22 were successfully sequenced. This left 5.4 Mb of corresponding human sequences undetectable in chimpanzee chromosome 22. Assuming the 5.4 Mb of DNA that was unable to be sequenced in the chimpanzee genome was 70% homologous to the corresponding human sequence (very generous for sequences that are not alignable!) and combining this with the 27 Mb of sequenced chimpanzee DNA (assuming this region is 95% homologous, see above) would give a homology of 90% for human chromosome 21 and chimpanzee chromosome 22...

What is the significance of 98.5% versus 90% homology? If the human and chimpanzee genomes are 10% different, it rules out the possibility that humans and chimpanzees evolved from a common ancestor. If the difference between the two genomes is 10% then the total number of differences in the DNA sequence would be approximately 300 million nucleotide bases (10% of 3 billion nucleotides present in humans or chimpanzees), meaning that 150 million bases in both the human and chimpanzee have mutated and been fixed in the population since the last common ancestor...

If the hypothetical divergence of humans and chimpanzees occurred about 5 million years ago and given that a human generation is about 20 years (and a chimp slightly less), then 250,000 generations have passed from the time humans and chimpanzees diverged from a common ancestor. To get 150 million nucleotide changes in 250,000 generations, the two lines of descent would require 600 beneficial mutations fixed in each population of ancestral humans and chimpanzee per generation. However, nearly all mutations are neutral, having no effect and therefore are not selectable, or are slightly deleterious, causing genetic deterioration in a population of organisms. A few beneficial mutations have been observed, such as mutations that confer antibiotic resistance in bacteria and sickle cell trait in humans."

http://www.icr.org/index.php?module=articles&action=print&ID=2324

What does all ot this mean? The mutation rate would have to be so high it would have threaten the homo line with extinction. There are only two viable alternatives for mutations being fixed in our genomes on this level. It was either relaxed functional constraint or adaptive evolution.

"If only 1,000 of the mutations are beneficial, then nearly all of the 150 million mutations in the human lineage would be slightly deleterious or neutral. Deleterious mutations would lead to degeneration of the genome resulting in extinction, and the neutral mutations would cause no change."

It should be realized that these calculations are based on the work of evolutionary biologists. The gross underestimation of the homology of chimpanzee and human functional DNA and the deleterious effects of mutations are the most signifigant errors in the Quiet Post Thread. I have debated Pete for some time and I know that he is aware of these problems. For whatever reason he did not factor them into his calculations. Had he done that I never would have started this thread, in fact, I would have gladly reped him for the effort and congradulated him on it. He didn't and it's not like he was unaware that these problems exist.

 

[Tomk80]

The implications of the mutation rate of the functional genome in bacteria being extended to hominid mutation rates left out two important factors.

1. The effects of deleterious mutations ranging from cell death to degenerative disease effecting overall populations.

This was never factored in even though this is the most common effect observed in phenotypes. The mutation must get through the cell cycle checkpoints, then get fixed in the genome and ultimatly create a new allele the creates a beneficial effect.

You've made that allegation more than once. So here is your chance to back it up. Correct the mathematical model Pete has made. Come on, show us the math!

[2. The homology of chimpanzee and human genomes is grossly over estimated.

At best the overall estimates are 95% (see Divergence between samples of chimpanzee and human DNA sequences is 5%, counting indels ) taking into account the indels Pete was well aware of. What is more over 20% of the protein coding sequences show gross structural changes, another fact Pete was well aware of. I know this because he pressed me to find in the chimpanzee chromosome 22/human chromosome 21 paper to show him where the functional part of the genome was effected, I found this:

"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.(see protein coding characterization in, Nature 429, 382 - 388 (27 May 2004) cited and linked in the Quite Post Thread)

The conservative estimate Pete used was on the effective genome. The 95% figure talks about the entire genome (which includes non-coding parts). The majority of the indel mutations were in non-coding parts, so that wouldn't change the figure much. Furthermore, changes in the splicing sites do not have to be big to still give rise to a gross structural change, in which case Pete's estimate of changes in the effective genome still wouldn't change.

The benefical mutation rate for hominids has been estimated for decades and evolutionists are desperatly trying to hide the fact that it is ridiculasly high to be the result of random mutations. I have deliberatly avoided creationist literature but I see no reason to continue quoting solely from secular sources since they are saying the exact same thing.

http://www.icr.org/index.php?module=articles&action=print&ID=2324

What does all ot this mean? The mutation rate would have to be so high it would have threaten the homo line with extinction. There are only two viable alternatives for mutations being fixed in our genomes on this level. It was either relaxed functional constraint or adaptive evolution.

"If only 1,000 of the mutations are beneficial, then nearly all of the 150 million mutations in the human lineage would be slightly deleterious or neutral. Deleterious mutations would lead to degeneration of the genome resulting in extinction, and the neutral mutations would cause no change."

It should be realized that these calculations are based on the work of evolutionary biologists. The gross underestimation of the homology of chimpanzee and human functional DNA and the deleterious effects of mutations are the most signifigant errors in the Quiet Post Thread. I have debated Pete for some time and I know that he is aware of these problems. For whatever reason he did not factor them into his calculations. Had he done that I never would have started this thread, in fact, I would have gladly reped him for the effort and congradulated him on it. He didn't and it's not like he was unaware that these problems exist.

Give me the scientific literature on this. Were have they estimated the beneficial mutation rate in humans? How does this rate hold up currently compared to 2 million years ago in their ancestors. You say this is known by evolutionists but hidden, but if it is known it should be found in the scientific literature. So cough up.

 

[mark kennedy]

You've made that allegation more than once. So here is your chance to back it up. Correct the mathematical model Pete has made. Come on, show us the math!

"Comparative DNA sequence studies between humans and nonhuman primates will be important for understanding the genetic basis of the phenotypic differences between these species. Here we compare ∼27 Mb of human chromosome 21 with chimpanzee DNA sequences identifying 57 genomic rearrangements (deletions and insertions ranging in size from 0.2 to 8.0 kb) between the two species. These rearrangements are distributed along the entire length of chromosome 21, with ∼35% found in genomic intervals encoding genes (genic intervals), and have occurred in the genomes of both humans and chimpanzees. "

Genomic DNA Insertions and Deletions Occur Frequently Between Humans and Nonhuman Primates

That is 25,000,000 bases with 35% being found in in genomic intervals coding genes. That is, unless my math is off, 875,000,000 bases in the coding portion of the gene.

The conservative estimate Pete used was on the effective genome. The 95% figure talks about the entire genome (which includes non-coding parts). The majority of the indel mutations were in non-coding parts, so that wouldn't change the figure much. Furthermore, changes in the splicing sites do not have to be big to still give rise to a gross structural change, in which case Pete's estimate of changes in the effective genome still wouldn't change.

The estimate in the chimpanzee consortiums paper estimated the gross stuctural changes being over 20% while the other one I just cited and linked puts the number of overall indels in the coding portions at 35%. I don't know if that takes into account the 1-2% of single base substitutions but I seriously doubt it.

Give me the scientific literature on this. Were have they estimated the beneficial mutation rate in humans? How does this rate hold up currently compared to 2 million years ago in their ancestors. You say this is known by evolutionists but hidden, but if it is known it should be found in the scientific literature. So cough up.

I have been giving you guys the scientific literature all along. This particular portion of the genome is showing a lot more indels then you want to admitt. Now if you can tell me the percentage of overall mutations would be benefical then we can determine if it is feasible that mutations can account for this. One thing is certain, mutation rates create a major problem for evolution and it will take some time for this to sink in since we have been told for so long that the genomes are virtually identical. The truth is coming in, its not that simple.

 

[Tomk80]

"Comparative DNA sequence studies between humans and nonhuman primates will be important for understanding the genetic basis of the phenotypic differences between these species. Here we compare ∼27 Mb of human chromosome 21 with chimpanzee DNA sequences identifying 57 genomic rearrangements (deletions and insertions ranging in size from 0.2 to 8.0 kb) between the two species. These rearrangements are distributed along the entire length of chromosome 21, with ∼35% found in genomic intervals encoding genes (genic intervals), and have occurred in the genomes of both humans and chimpanzees. "

Genomic DNA Insertions and Deletions Occur Frequently Between Humans and Nonhuman Primates

That is 25,000,000 bases with 35% being found in in genomic intervals coding genes. That is, unless my math is off, 875,000,000 bases in the coding portion of the gene.

Sorry, but that doesn't answer the question in any way.

The estimate in the chimpanzee consortiums paper estimated the gross stuctural changes being over 20% while the other one I just cited and linked puts the number of overall indels in the coding portions at 35%. I don't know if that takes into account the 1-2% of single base substitutions but I seriously doubt it.

No Mark, 20% of the proteins are altered. That is a completely different number from the 98.5% difference in that it is talking about an entirely different thing. You are comparing apples and oranges.

I have been giving you guys the scientific literature all along. This particular portion of the genome is showing a lot more indels then you want to admitt. Now if you can tell me the percentage of overall mutations would be benefical then we can determine if it is feasible that mutations can account for this. One thing is certain, mutation rates create a major problem for evolution and it will take some time for this to sink in since we have been told for so long that the genomes are virtually identical. The truth is coming in, its not that simple.

Sorry Mark, but in all your time you have never given any evidence backing up your statements. All you have given were articles you didn't understand yourself.

 

[mark kennedy]

Sorry, but that doesn't answer the question in any way.

Yes it did and there is a whole lot more coming out besides. Now that is 35% of the coding genes consisting of indels. If the simularity of two totally different genus of primates is convincing proof of common ancestory then differences this vast should be proof of independant lineage. If 5% of the genomes are different 300 million nucleotide bases (5% of 3 billion nucleotides present in humans or chimpanzees), meaning that 75 million bases in both the human and chimpanzee have mutated and been fixed in the population since the last common ancestor 5-10 million years ago. Most of the most important changes starting 2 1/2 million years ago and ending about 1/2 million years ago.

You said:

You've made that allegation more than once. So here is your chance to back it up. Correct the mathematical model Pete has made. Come on, show us the math!

I replied:

That is 25,000,000 bases with 35% being found in in genomic intervals coding genes. That is, unless my math is off, 875,000,000 bases in the coding portion of the gene.

I asked you for the mutation rate accounting for the neutral with would be around 80% and the deleterious mutations that would probably out number the beneficial ones. That is in addition to:

"If only 1,000 of the mutations are beneficial, then nearly all of the 150 million mutations in the human lineage would be slightly deleterious or neutral.

Now if you know how the mutation rate is any different then 1 in 1000 being beneficial I have yet to see a single source document supporting it.

No Mark, 20% of the proteins are altered. That is a completely different number from the 98.5% difference in that it is talking about an entirely different thing. You are comparing apples and oranges.

That is 20% of the protein coding genes showing gross structural changes while 35% of the protein coding just consisting of indels. I realize that we are not talking about the same thing because you are not talking about nucleotide or amino acid sequences, you are talking about nucleotide identity.

"For those 179 genes, the average nucleotide and amino acid identity in the coding region is 99.29% and 99.18%, respectively. Of these, 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"

Thats an almost identical average but only 39 genes show an identical amino acid sequences and only seven are identical at a nucleotide sequence level. No, we are not talking about the same thing, you want to confuse superfical simularities with coding sequences.

Sorry Mark, but in all your time you have never given any evidence backing up your statements. All you have given were articles you didn't understand yourself.

Sorry yourself, you have offered nothing in the way of substantive or empircal evidence to determine your assertions. The arguments offered are usually a couple of lines long and ignore the evidence at hand. The mutation rate Pete was using did not take into account the neutral and deleterious effects, even though they would vastly outnumber the rare beneficial effect. What is more, even in bacteria the beneficial effects of mutations only a small percentage of the population for a short time.

By the way, the 68,000 indels are only in the comparision of the two chromosomes HSA21 and PTR22. There are only Two hundred and twenty-five genes in the this, the smallest chromosome in the human genome. Still, this small segment of the human genome is thought to be responsible for the characteristics that make us uniquely human. There have been observed and demonstrated effects of alterations to these genes, down syndrome being the most common.

 

[gluadys]

By the way, the 68,000 indels are only in the comparision of the two chromosomes HSA21 and PTR22. There are only Two hundred and twenty-five genes in the this, the smallest chromosome in the human genome. Still, this small segment of the human genome is thought to be responsible for the characteristics that make us uniquely human. There have been observed and demonstrated effects of alterations to these genes, down syndrome being the most common.

Where does the paper make the assertion I have bolded?

 

[mark kennedy]

Where does the paper make the assertion I have bolded?

That was not a quote, it was an allusion to the intent of the paper:

"Human–chimpanzee comparative genome research is essential for narrowing down genetic changes involved in the acquisition of unique human features, such as highly developed cognitive functions, bipedalism or the use of complex language. Here, we report the high-quality DNA sequence of 33.3 megabases of chimpanzee chromosome 22."

And the opening discussion of the characterization of the specific genes in these chromosomes:

"Moreover, molecular analysis of HSA21 and its genes is of central medical interest because of trisomy 21, the most common genetic cause of mental retardation in the human population. One case of trisomy 22 in chimpanzee has been reported, with phenotypic features similar to human Down's syndrome"

They can learn what gene do by what happens when they don't work properly