Do Chimps and Humans Share a Common Ancestor? Primer for a formal debate

[sfs]

No one predicted the indels and the link you provided does not calculate the mutation rate. Lets do this again since you have so much trouble following my main point. There are five million indels in 5 million years in addition to the single base substitutions you describe in the link. These indels add up to something like 90 Mb.

That is one indel per year for 5 million years. Sounds pretty consistent with known mutation rates does it not?

Yes, it does.

That means all of us have 20 indels, with a mean average of 280 base pairs involved.

Correct. (There's a factor of two here that cancels: half of the indels were in the chimpanzee lineage, so it's 10 indels per generation in each lineage, but each of us has two copies of the genome. So divide by two and then multiply by two.)

 

[mark kennedy]

Yes, it does.

Correct. (There's a factor of two here that cancels: half of the indels were in the chimpanzee lineage, so it's 10 indels per generation in each lineage, but each of us has two copies of the genome. So divide by two and then multiply by two.)

So are you honestly saying that no accelerated evolution is required? It is very curious since you still don't really have a mutation rate for indels the question arises, what are the mutational forces responsible?

Now I'll buy that the single base substitutions seem to be lining up with the mutation rate. I guess if you assume that a high number of these mutations are becoming permanently fixed as we speak there is no problem. I do see a problem with indels, particularly since it's harder to find indels then single base substitutions.

The fact of the matter is no one expected to find these indels, because they are not happening on this scale. I think you guys know this and it's fascinating to watch them rationalized away.

I know your not interested Steve but I would be delighted to debate this with you formally. If not I suppose I will be forced to just refute the same tired old Talk Origins nonsense.

By the way, what is the mutation rate for Homo sapien sapiens again? Last time I asked you gave me three.

 

[Tomk80]

So are you honestly saying that no accelerated evolution is required? It is very curious since you still don't really have a mutation rate for indels the question arises, what are the mutational forces responsible?

You do not need a mutation rate to find out causes that are most likely most important in mutations. All you need for that is a an assessment of which differences there are quantitatively in the genome. Such estimates are found quite quickly. This was the first one I found when looking for it. Unfortunately I could so far only get the abstract for this article, but from that it seems that the main reason for indels in humans are repititive sequences. The copying machinery just skips a beat here, and because the sequence is repetitive, the machinery checking the patterns also more easily misses an insertion or deletion. This article also supports this conclusion.

Given that we use Single Tandem Repeat Polymorphisms to identify people in crime research, and given that these are quite specific and the result of indel mutations and given that these STRPs are not the only sources of variation in genome lenght, it would seem to me that 1 mutation per year may be on the low side of the real indel mutation rate in the population.

Now I'll buy that the single base substitutions seem to be lining up with the mutation rate. I guess if you assume that a high number of these mutations are becoming permanently fixed as we speak there is no problem. I do see a problem with indels, particularly since it's harder to find indels then single base substitutions.

I don't follow this reasoning. Because the methodology for detecting indels is harder than for detecting substitutions they cannot be in line with the mutation rate? How does that work?

The fact of the matter is no one expected to find these indels, because they are not happening on this scale. I think you guys know this and it's fascinating to watch them rationalized away.

No, they were not expected because we are not omniscient. If you look at the current literature (for example the articles above), you can find that indels are actually quite common. However, they are harder to detect because they require more than just lining up the sequences.

I know your not interested Steve but I would be delighted to debate this with you formally. If not I suppose I will be forced to just refute the same tired old Talk Origins nonsense.

By the way, what is the mutation rate for Homo sapien sapiens again? Last time I asked you gave me three.

Depends on which one you want. Measures of mutation rates vary considerably according to the way they are measured, as well as which mutations you are talking about..

 

[sfs]

So are you honestly saying that no accelerated evolution is required?

I'm saying that there is no evidence that an increased rate of mutation, or of neutral substitution, is required. ("Accelerated evolution" can mean a variety of things. In one sense, there likely has been accelerated evolution in the human lineage: proteins have evolved faster in human ancestors than in most primates, because human ancestors had such a small effective population size that more mildly deleterious mutations could accumulate in our lineage. In other words, humans are a little more defective than the average primate.)

It is very curious since you still don't really have a mutation rate for indels the question arises, what are the mutational forces responsible?

Your question makes no sense in this context. You were the one making a claim, that there was some kind of problem for evolution in the number of indel differences between humans and chimpanzees. The actual situation is that the number of differences seems to be consistent with what we can tell about the indel mutation rate from studies within humans. This is the point at which you should start offering some evidence for your claim, rather than asking me about the causes of indel mutations. (And yes, many of the mutational forces are known: slippage during replication, nonhomologous recombination between low-copy repeats, transposon insertions.)

Now I'll buy that the single base substitutions seem to be lining up with the mutation rate. I guess if you assume that a high number of these mutations are becoming permanently fixed as we speak there is no problem.

There's no problem whether you make that assumption or not. The chimpanzee genome paper didn't look primarily at fixed differences, but at the difference between a single chimpanzee genome and a single human genome, without checking whether those differences are fixed in either population. (The assumption you speak of happens to be one of the most basic results in population genetics and is undoubtedly more or less correct, but it is not necessary here.)

I do see a problem with indels, particularly since it's harder to find indels then single base substitutions.

When are you going to articulate this problem and provide evidence for its existence?

The fact of the matter is no one expected to find these indels, because they are not happening on this scale.

No, the fact of the matter is that we didn't expect to find this many indels because we didn't know what to expect. That's why we measure things in science: to learn new things. If we only ever found what we already expected, we'd all be bored to tears -- we'd quit and become stock brokers or surfers or something. (And it's not like the expectations were off by orders of magnitude; the observed number is about twice as large as might have been predicted, based on the crude knowledge of indels available at the time.)

The bit about indels not happening on this scale is something you made up. If indel mutations don't happen on this scale, why are there millions of indels that differ between individual humans? Where did they come from? And what is your evidence that they don't happen on this scale?

I think you guys know this and it's fascinating to watch them rationalized away.

I think you're a bowl of chocolate pudding with whipped cream and a cherry on top. Thinking something doesn't make it so.

I know your not interested Steve but I would be delighted to debate this with you formally. If not I suppose I will be forced to just refute the same tired old Talk Origins nonsense.

You are correct: I am not interested.

By the way, what is the mutation rate for Homo sapien sapiens again? Last time I asked you gave me three.

Look up my previous answer: my knowledge of the mutation rates hasn't changed since then, and I don't see any reason to do the calculation again.

 

[karzma]

hmm interesting

 

[mark kennedy]

I'm saying that there is no evidence that an increased rate of mutation, or of neutral substitution, is required. ("Accelerated evolution" can mean a variety of things. In one sense, there likely has been accelerated evolution in the human lineage: proteins have evolved faster in human ancestors than in most primates, because human ancestors had such a small effective population size that more mildly deleterious mutations could accumulate in our lineage. In other words, humans are a little more defective than the average primate.)

There are 49 regions of accelerated evolution that include functionally important genes:

Human accelerated regions (HARs), first described in August 2006, are a set of 49 segments of the human genome which are conserved throughout vertebrate evolution but are strikingly different in humans. They are named HAR1 through HAR49 according to their degree of difference between humans and chimpanzees (HAR1 showing the largest degree of human-chimpanzee differences of the 49). Found by scanning through giant genomic databases of multiple species, some of these highly mutated areas are thought to have contributed to the development of human neuroanatomy, language, and complex thought.

Several of the HARs encompass genes known to produce proteins important in neurodevelopment. HAR1 is an 118 base pair stretch found on the long arm of chromosome 20 overlapping with part of the RNA genes HAR1F and HAR1R. HAR1F is active in the developing human brain. The HAR1 sequence is found (and conserved) in chickens and chimpanzees but is not present in fish or frogs that have been studied. There are 18 base pair mutations different between humans and chimpanzees, far more than expected by its history of conservation​

Human Accelerated Regions

Your question makes no sense in this context. You were the one making a claim, that there was some kind of problem for evolution in the number of indel differences between humans and chimpanzees. The actual situation is that the number of differences seems to be consistent with what we can tell about the indel mutation rate from studies within humans. This is the point at which you should start offering some evidence for your claim, rather than asking me about the causes of indel mutations. (And yes, many of the mutational forces are known: slippage during replication, nonhomologous recombination between low-copy repeats, transposon insertions.)

There's no problem whether you make that assumption or not. The chimpanzee genome paper didn't look primarily at fixed differences, but at the difference between a single chimpanzee genome and a single human genome, without checking whether those differences are fixed in either population. (The assumption you speak of happens to be one of the most basic results in population genetics and is undoubtedly more or less correct, but it is not necessary here.)

Ok, first we are 99% the same as chimpanzees, then its 95%. Upon finding out that we are actually much more different the required mutation rate is not effected, which is absurd. Then after a long line of being told this nonsense, even in the announcement of the Chimpanzee Genome paper the statistical comparison remains the same. Why, because they only want to count the single base substitutions that would be required.

Now, I'll be happy to provide whatever evidence is avaiable to me here but I'm asking a Broad Institute staff scientist to do a very basic calculation, what was the overall mutation rate. You can do it in your head, I know you are more then capable so what's the problem?

When are you going to articulate this problem and provide evidence for its existence?

First of all mutations of length do not occur in highly conserved genes involved in neurological development, with a positive effect on the level required. What is more you neutral and slightly deleterious model does not take into consideration the level of alterations needed on a per annum basis.

The mutation rate you showed in you brief discussion on while true is not complete. What about the indels Steve, why did you not iinclude them in your discussion?

No, the fact of the matter is that we didn't expect to find this many indels because we didn't know what to expect. That's why we measure things in science: to learn new things. If we only ever found what we already expected, we'd all be bored to tears -- we'd quit and become stock brokers or surfers or something. (And it's not like the expectations were off by orders of magnitude; the observed number is about twice as large as might have been predicted, based on the crude knowledge of indels available at the time.)

Fair enough, I'm not trying to make a big point based on something surprising found during a large research project. Of course you should expect surprises and many people are attached to this kind of work for that reason. I'm just saying, once the differences are identified it should be simple enough to calculate the rate at which they were accumulated.

Something else even more important. There has to be a molecular mechanism for overhauling highly conserved genes. We both know that random mutations are not going to triple the size of the human brain with the requisite proportional adaptations know to have had to happen. It's fine to say you don't know what they are but wrong to insist that random mutations are an explanation.

The bit about indels not happening on this scale is something you made up. If indel mutations don't happen on this scale, why are there millions of indels that differ between individual humans? Where did they come from? And what is your evidence that they don't happen on this scale?

You left out the most important consideration in evolutionary biology. What about the known effects of these indels. You can find a lot of examples of disease and disorder but large scale adaptations are rare at best. In fact when it comes to an inframe indel they are virutally nonexistant.

I didn't make this up and you are no stranger to the deleterious effects of mutations on genes involved in neural development.

I think you're a bowl of chocolate pudding with whipped cream and a cherry on top. Thinking something doesn't make it so.

Just like serendipitous effects from random mutations on human brain cells are wishful thinking.

You are correct: I am not interested.

What if I promised never to make this argument about the mutation rate being vastly exceeded by the known differences on this or any other discussion board. Is that even remotely appealing?

Look up my previous answer: my knowledge of the mutation rates hasn't changed since then, and I don't see any reason to do the calculation again.

I have looked at them and can't seem to cross reference them with peer reviewed scientific publication, so I persist.

The inverse logic is intuitively obvious, if homology is proof for common ancestry then the differences are proof against. You may not like that, you may not accept that, you may not want to admit it but you know it none the less.

What are the effects of random mutation on the human brain when they have an effect strong enough for natural selection to act Steve?

 

[Chalnoth]

Just like serendipitous effects from random mutations on human brain cells are wishful thinking.

No. It's where natural selection comes in. When you have a reasonably large population, and a particular trait is selected for rather strongly (in this case greater intelligence), then you are virtually guaranteed that somebody in the population will get a beneficial mutation that effects the trait in question. The mutation is then highly likely to spread through the population via sexual reproduction.

The search for the HAR's is a search for discovering what sorts of selective pressures are ancestors were under.

 

[sfs]

There are 49 regions of accelerated evolution that include functionally important genes[...]

Complete change of subject, Mark. You're supposed to be explaining why the overall rate of indel differences between humans and chimpanzees is incompatible with known mutation rates. Why aren't you doing that? You were very condescending when you said you were going to do it. Get started already.

Ok, first we are 99% the same as chimpanzees, then its 95%. Upon finding out that we are actually much more different the required mutation rate is not effected, which is absurd.

As has been explained to you many times, the 99% and the 95% are measuring different things. The 99%, which is the rate of single-base substitution differences between humans and chimps, is explained very well by the known single-base substitution rate in humans, and is as predicted. The 95%, which includes the indel differences, could not be predicted because the indel mutation rate in humans was (and still is) unknown; the only thing we know now is that it is higher than we guessed it was ten years ago, and that indels contribute substantially more genetic variation to humans than single-base substitutions do. So the human/chimpanzee result is entirely compatible with other indirect evidence about the indel mutation rate, but we can't do a quantitative comparison yet.

You're supposed to be explaining why the overall rate of indel differences between humans and chimpanzees is not compatible with known mutation rates. Why aren't you doing that?

Then after a long line of being told this nonsense, even in the announcement of the Chimpanzee Genome paper the statistical comparison remains the same. Why, because they only want to count the single base substitutions that would be required.

Because they were writing for readers who can handle the existence of more than a single value to be measured.

Now, I'll be happy to provide whatever evidence is avaiable to me here

Don't talk about what you're going to do -- do it. Just provide the evidence already. You implied that it would be easy to show that there's a problem. Why aren't you doing so?

but I'm asking a Broad Institute staff scientist to do a very basic calculation, what was the overall mutation rate. You can do it in your head, I know you are more then capable so what's the problem?

The problem is that I've already done the calculation for you multiple times. They say that the definition of insanity is doing the same thing over and over again and expecting diffferent results. I'm not insane, and I don't expect repeating the same calculation again is going to make any difference to you. If you really want my calculation, just find my last post on the subject.

Why do you want my calculation, anyway? You said you were going to show why there is a problem for evolution in the rate of indels between humans and chimpanzees. Presumably you already knew what you were going to say. Why don't you say it?

First of all mutations of length do not occur in highly conserved genes involved in neurological development, with a positive effect on the level required.

Change of subject. Subject: overall rate of indels. Your job: explain why it's a problem.

What is more you neutral and slightly deleterious model does not take into consideration the level of alterations needed on a per annum basis.

My model takes the number of observed differences and divides by the number of years. How does that fail to take into account the number needed per year?

The mutation rate you showed in you brief discussion on while true is not complete. What about the indels Steve, why did you not iinclude them in your discussion?

I explicitly left them out of my discussion in the Quiet Thread because not enough was known about the indel mutation rate to make useful predictions, a fact that I've already repeated in this thread. You're still not explaining why there's a problem here, Mark.

Fair enough, I'm not trying to make a big point based on something surprising found during a large research project. Of course you should expect surprises and many people are attached to this kind of work for that reason. I'm just saying, once the differences are identified it should be simple enough to calculate the rate at which they were accumulated.

Of course it's simple to calculate the rate at which they accumulated. But you're claiming that rate is inconsistent with known mutation rates. Why? What is your evidence?

Something else even more important. There has to be a molecular mechanism for overhauling highly conserved genes.[...]

Change of subject again. Please post your evidence that the indel differences are inconsistent with known mutation rates.

[More comments, in which does not present his evidence, deleted.]

What if I promised never to make this argument about the mutation rate being vastly exceeded by the known differences on this or any other discussion board. Is that even remotely appealing?

Nope.

The inverse logic is intuitively obvious, if homology is proof for common ancestry then the differences are proof against.

Intuitively obvious but completely wrong. I differ genetically from my parents, due to new mutations. You take that as evidence that I'm not descended from them? And how does this show that the overall rate of indels is too high for mutation to explain?

What are the effects of random mutation on the human brain when they have an effect strong enough for natural selection to act Steve?

Change of subject again. Do what you said you'd do, Mark.

 

[Brennin]

Do Chimps and Humans Share a Common Ancestor?

I remain incredulous.

 

[karzma]

we need a time machine

 

[mark kennedy]

I'm saying that there is no evidence that an increased rate of mutation, or of neutral substitution, is required. ("Accelerated evolution" can mean a variety of things. In one sense, there likely has been accelerated evolution in the human lineage: proteins have evolved faster in human ancestors than in most primates, because human ancestors had such a small effective population size that more mildly deleterious mutations could accumulate in our lineage. In other words, humans are a little more defective than the average primate.)

Simply amazing, natural selection of slightly more defective repair mechanisms. There are accelerated regions and this is not difficult to find in the scientific literature.

Indeed, as first recognized by Charles Darwin, adaptive evolution must have played a key role in driving the acquisition of greater cognitive powers in humans (Darwin, 1871). It is therefore reasonable to suppose that positive selection on genes involved in nervous system biology should have operated more intensely during the descent of humans than in species showing less dramatic cognitive evolution. However, researchers have not been able to make a priori predictions regarding how intensified selection on the nervous system might have molded the molecular evolution of the primate genome. (Accelerated Evolution of Nervous System
Genes in the Origin of Homo sapiens, Cell, Vol. 119, 1027–1040, December 29, 2004)

Slightly deleterious do not account for an overhaul of highly conserved genes and you know it.When you add all of this up you are looking at 145 Mb that include single nucleotide substitutions, indels and major chromosomal rearrangements (4.8%) Random mutations do not account for this and any attempt to reconcile adaptive spikes with spontaneous mutation rates is utter folly.

A total of 585 of the 13,454 human–chimpanzee orthologues (4.4%) have observed KA/KI > 1. However, given the low divergence, the KA/KI statistic has large variance. Simulations show that estimates of KA/KI > 1 would be expected to occur simply by chance in at least 263 cases if purifying selection is allowed to act non-uniformly across genes.” (The Initial Sequence of the Chimpanzee Genome, Nature 2005)

Your question makes no sense in this context. You were the one making a claim, that there was some kind of problem for evolution in the number of indel differences between humans and chimpanzees. The actual situation is that the number of differences seems to be consistent with what we can tell about the indel mutation rate from studies within humans. This is the point at which you should start offering some evidence for your claim, rather than asking me about the causes of indel mutations. (And yes, many of the mutational forces are known: slippage during replication, nonhomologous recombination between low-copy repeats, transposon insertions.)

The human and chimpanzee genomes show structural differences as well, ranging in scale from local events to large-scale chromosomal alterations. Sequence inversions between humans and chimpanzees are estimated at over 1500 events, ranging in size from 23 bp to as large as 62 Mb. Cheng et al. identified 296 regions in the human genome showing significant copy number increases in humans compared to chimpanzees. These segmental duplications span 7.2 Mb and are preferentially located in pericentromeric regions and on chromosomes 5 and 15 What makes us human: revisiting an age-old question in the genomic era
Nitzan Mekel-Bobrov and Bruce T Lahn

It's not like you are unaware that all of these changes are cumulative. This is in addition to 6 single base substitutions and one indel per year for 5 million years. Then you just pretend this is perfectly normal when clearly it is not. The evidence is not only available, it's overwelming.

There's no problem whether you make that assumption or not. The chimpanzee genome paper didn't look primarily at fixed differences, but at the difference between a single chimpanzee genome and a single human genome, without checking whether those differences are fixed in either population. (The assumption you speak of happens to be one of the most basic results in population genetics and is undoubtedly more or less correct, but it is not necessary here.)

The Chimpanzee paper did mention that most of the differneces were fixed. The same is going to hold true for the rearrangements and the indels I'm sure. I don't have a problem with occasionally a mutation becoming fixed dispite the physiological costs. It's when it doesn't matter what the evidence is you act as if it's perfectly normal.

When are you going to articulate this problem and provide evidence for its existence?

Sure, lets do this again Steve. Lets start with 20 indels per generation, which is 280 base pairs. Then you have the 120 base pairs from the single base substitutions. Then you can factor in the chromosomal rearrangements which lag behind in terms of base pairs but but we are looking at another 80 base pairs. No way this calls for accelerated mutation rates.

I know what your thinking, so what's the problem? The problem is that this does not happen and bear in mind genes are being effected as well:

It has been suggested that humans may suffer a high genomic deleterious mutation rate. Here we test this hypothesis by applying a variant of a molecular approach to estimate the deleterious mutation rate in hominids from the level of selective constraint in DNA sequences. 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, indicating that the effects of deleterious mutations may have combined synergistically. Furthermore, the level of selective constraint in hominid protein-coding sequences is atypically low. A large number of slightly deleterious mutations may therefore have become fixed in hominid lineages.(High genomic deleterious mutation rates in hominids.Centre for the Study of Evolution and School of Biological Sciences, University of Sussex, Brighton, UK. A.C.Eyre-Walker@susx.ac.uk)​

Every single paper I am gleaning from the net is saying that accelerated evolution is required but you keep saying the exact opposite. I have no idea why.

No, the fact of the matter is that we didn't expect to find this many indels because we didn't know what to expect. That's why we measure things in science: to learn new things. If we only ever found what we already expected, we'd all be bored to tears -- we'd quit and become stock brokers or surfers or something. (And it's not like the expectations were off by orders of magnitude; the observed number is about twice as large as might have been predicted, based on the crude knowledge of indels available at the time.)

The bit about indels not happening on this scale is something you made up. If indel mutations don't happen on this scale, why are there millions of indels that differ between individual humans? Where did they come from? And what is your evidence that they don't happen on this scale?

For one thing I don't think you guys have had a crude knowledge of DNA or mutations for at least a half a century. You have had a complete human genome sequence and the indels don't come up until the chimpanzee genome is being compared to the human genome.

What is even more important is that you know they don't happen on that scale. The divergence of my genome and yours is less then 1% and the same holds true for any two human beings on the planet. The mutation rates indicated by every researcher I have ever seen calculate it does not indicate hundreds of mutations per generation as they would have to to account for the differences between chimpanzees and humans.

I didn't make this stuff up and you know it.

I think you're a bowl of chocolate pudding with whipped cream and a cherry on top. Thinking something doesn't make it so.

Just like thinking that benefical effects from random mutations are going to overhaul functionally biased neural genes.

Look up my previous answer: my knowledge of the mutation rates hasn't changed since then, and I don't see any reason to do the calculation again.

It's still the same as it was before and it does not account for the indels.

 

[mark kennedy]

Double post, I'm not kidding the internet here is just plain awful.

 

[Chalnoth]

we need a time machine

Why? We have fossils and DNA. We need nothing more to demonstrate that humans and other animals share a common ancestry.

 

[Chalnoth]

Simply amazing, natural selection of slightly more defective repair mechanisms. There are accelerated regions and this is not difficult to find in the scientific literature.

And so are you going to bother to respond to my very clear response to this issue a few posts back? Accelerated regions are not a problem for evolution. On the contrary, they are an expectation.

 

[USincognito]

I'll address the fossil post from a few pages back tonight when I have some free time.

And so are you going to bother to respond to my very clear response to this issue a few posts back? Accelerated regions are not a problem for evolution. On the contrary, they are an expectation.

A simple Google of "human accelerated region evolution" calls up a number of blog entires and journal and mainstream press articles on how HARs and specifically HAR1 are evidence for evolution, not the magic bullet that will kill it like Mark thinks.

It's been a year or so since he started going on (and on and on) about HAR1 and I asked him why he didn't contact the authors of the article that appeared in Nature. He brushed it off and I suppose never got around to following up. I figured at the very least, if he's got the stones to tell a geneticist like sfs, he doesn't know anything about genetics, he'd gather the gumption of writing them, and at least have them lie to his face (since that's his claim) then just tell tales about them out of school.

 

[sfs]

Simply amazing, natural selection of slightly more defective repair mechanisms.

I didn't suggest that humans had more defective repair mechanisms. I don't know what you're talking about.

There are accelerated regions and this is not difficult to find in the scientific literature.

Of course there are. But we're not talking about a few accelerated regions, we're talking about genome-wide rates of insertions and deletions, and why you think they pose a major problem for evolution. Why do you keep inserting these irrelevancies?

[Irrelevant material deleted.]

Slightly deleterious do not account for an overhaul of highly conserved genes and you know it.

But we're not talking about the overhaul of highly conserved genes; we're talking about the overall rate of indels. When are you finally going to present your killer argument about that?

When you add all of this up you are looking at 145 Mb that include single nucleotide substitutions, indels and major chromosomal rearrangements (4.8%) Random mutations do not account for this and any attempt to reconcile adaptive spikes with spontaneous mutation rates is utter folly.

It's utter folly, and yet you seem to be unable to say why it's utter folly. Don't just keep repeating your original claim, Mark: offer an actual argument about why this is utter folly.

[More seemingly random bits of genetics deleted. ]

It's not like you are unaware that all of these changes are cumulative. This is in addition to 6 single base substitutions and one indel per year for 5 million years. Then you just pretend this is perfectly normal when clearly it is not. The evidence is not only available, it's overwelming.

The evidence is clear, it's available, it's overwhelming, but you're somehow unable to post it, after years of talking about it. Please excuse my skepticism.

The Chimpanzee paper did mention that most of the differneces were fixed. The same is going to hold true for the rearrangements and the indels I'm sure. I don't have a problem with occasionally a mutation becoming fixed dispite the physiological costs. It's when it doesn't matter what the evidence is you act as if it's perfectly normal.

?? The vast majority of mutations have no physiological effect, and therefore no cost.

Sure, lets do this again Steve. Lets start with 20 indels per generation, which is 280 base pairs. Then you have the 120 base pairs from the single base substitutions. Then you can factor in the chromosomal rearrangements which lag behind in terms of base pairs but but we are looking at another 80 base pairs. No way this calls for accelerated mutation rates.

Right.

I know what your thinking, so what's the problem? The problem is that this does not happen

Here's where your argument belongs, Mark. What is the evidence that this doesn't happen? What mutation rate is needed to explain the chimpanzee genome comparison for substitutions? For indels?
Using your numbers above, you're saying there need to be 120 new substitution mutations per human birth. That's just about exactly what we measure, so that works, right? Then there have to be 17 new insertions or deletions per human birth too, right (based on the chimpanzee genome finding that indels occur at 1/7th the rate of single-base substitutions)? (Call it 20, as you do above, if you want.) Back in the days before the chimpanzee genome, we used to think that indels occurred about one-tenth as often as single-base substitutions. The chimpanzee comparison showed that we were underestimating the number substantially, so that instead of there being 12 new mutations per person there are actually 17. It's nice to have a more accurate number, but why is 17 utterly absurd when 12 wasn't, and when you're already swallowing 120 other mutations?

and bear in mind genes are being effected as well:

It has been suggested that humans may suffer a high genomic deleterious mutation rate. Here we test this hypothesis by applying a variant of a molecular approach to estimate the deleterious mutation rate in hominids from the level of selective constraint in DNA sequences. 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, indicating that the effects of deleterious mutations may have combined synergistically. Furthermore, the level of selective constraint in hominid protein-coding sequences is atypically low. A large number of slightly deleterious mutations may therefore have become fixed in hominid lineages.(High genomic deleterious mutation rates in hominids.Centre for the Study of Evolution and School of Biological Sciences, University of Sussex, Brighton, UK. A.C.Eyre-Walker@susx.ac.uk)​

Every single paper I am gleaning from the net is saying that accelerated evolution is required but you keep saying the exact opposite. I have no idea why.

Probably because you don't understand what you're reading. I already noted in one post that humans probably have experienced accelerated protein evolution due to accumulating deleterious alleles (the result of a small population size). Did you miss that? I also pointed out that this effect has nothing to do with what you said you were going to do, which was show that the overall rate of indels in humans is too high for known mutation rates.

For one thing I don't think you guys have had a crude knowledge of DNA or mutations for at least a half a century. You have had a complete human genome sequence and the indels don't come up until the chimpanzee genome is being compared to the human genome.

So tell me, Mark, since you seem to know more about genetics than those of us in the field: how would you go about finding indels using just the complete human genome sequence?

 

[Split Rock]

When are you finally going to present your killer argument about that?

It's utter folly, and yet you seem to be unable to say why it's utter folly. Don't just keep repeating your original claim, Mark: offer an actual argument about why this is utter folly.

The evidence is clear, it's available, it's overwhelming, but you're somehow unable to post it, after years of talking about it. Please excuse my skepticism.

This is Mark's usual tactic.

1. Repeat an assertion over and over and never provide evidence to back it up.

2. Finally stop posting for a while after saying how much fun it was pulling our tail.

3. Post over in the Creationist-Only subforum about how we couldn't respond to his assertions.

4. Return later and post the same assertions without providing evidence.

rinse, repeat...etc.

 

[mark kennedy]

I'll address the fossil post from a few pages back tonight when I have some free time.



A simple Google of "human accelerated region evolution" calls up a number of blog entires and journal and mainstream press articles on how HARs and specifically HAR1 are evidence for evolution, not the magic bullet that will kill it like Mark thinks.

What it should bring up is a regulatory gene, 118 nucleotides long with 18 substitutions. This regulatory gene is involved in the development of the human cortex. But of course you knew that.

It's been a year or so since he started going on (and on and on) about HAR1 and I asked him why he didn't contact the authors of the article that appeared in Nature. He brushed it off and I suppose never got around to following up. I figured at the very least, if he's got the stones to tell a geneticist like sfs, he doesn't know anything about genetics, he'd gather the gumption of writing them, and at least have them lie to his face (since that's his claim) then just tell tales about them out of school.

First of all, I never said that the article was in error. I cited and quoted it but it was only recently that I was actually able to obtain the article. For the last 16 months I have been on active duty and I am currently serving in Iraq where the internet is far from reliable.

If you want to call me a liar then don't do it in the third person, tell me right here. I'm not shy about telling a liar what they are to their face. Nature, for instance, lied about the amount of DNA that is the same between the chimpanzee and humans.

For the umpteenth time, evolutionists will get it right in their peer reviewed publications but other then that I don't trust a word they say.

 

[mark kennedy]

I didn't suggest that humans had more defective repair mechanisms. I don't know what you're talking about.

That was a remark about the slightly deleterious model you are working from.

Of course there are. But we're not talking about a few accelerated regions, we're talking about genome-wide rates of insertions and deletions, and why you think they pose a major problem for evolution. Why do you keep inserting these irrelevancies?

Ok, you have never discussed the evolution of the human brain so why should I expect you to now? Pick a mutation rate:

2.5 x 10^-8 for all mutations
2.3 x 10^-9 for length mutations
2.3 x 10^-8 for all nucleotide substitutions

(Estimate of the Mutation Rate per Nucleotide in Humans. Genetics, Sept 2000)

Now you have 35 million substitutions in 5 million years, that is 140 per generation. Is that what this mutation rate predicts Steve?

[Irrelevant material deleted.]

Not all of it, you still have not dismissed the mutation rate of indels. Of course it lines up with scientific predictions so you should have no problem with it.

But we're not talking about the overhaul of highly conserved genes; we're talking about the overall rate of indels. When are you finally going to present your killer argument about that?

When you finally tell me what the mutation rate would have to be for 90 Mb to accumulate. You can add, divided, multiply or use calculus for all I care. Just show me in the considerable research that has been going on for the last half a century what the mutation rate was when the differences amounted to 1% and what they are now that it is below 5%.

It's utter folly, and yet you seem to be unable to say why it's utter folly. Don't just keep repeating your original claim, Mark: offer an actual argument about why this is utter folly.

I am but you keep dodging the question. You want me to argue but you don't want me to actually use the evidence. Pick a mutation rate, if you don't like the one I just offered then concoct one off the top of your head. Then you tell me the difference between 35 million base pairs in 5 million years and 145 million base pairs in 5 million years.

The mutation rate changes somewhat does it not?

[More seemingly random bits of genetics deleted. ]

I call it search and traverse but no matter.

The evidence is clear, it's available, it's overwhelming, but you're somehow unable to post it, after years of talking about it. Please excuse my skepticism.

When you honestly admit to a mutation rate and apply it to 99% the same and 94% the same I will show you the argument. It's not that you don't know what it is, you want the evidence before you make a prediction. Then you are going to act like that's what you expected all along just like you did with the differences in the DNA

?? The vast majority of mutations have no physiological effect, and therefore no cost.

Genes had to be overhauled for the human brain to triple in size Steve. Sooner or later something has to create a human brain. Either it came from an African ape or God. Identify the molecular mechanism and we can forget about these mutations.

Right.
Here's where your argument belongs, Mark. What is the evidence that this doesn't happen? What mutation rate is needed to explain the chimpanzee genome comparison for substitutions? For indels?
Using your numbers above, you're saying there need to be 120 new substitution mutations per human birth. That's just about exactly what we measure, so that works, right? Then there have to be 17 new insertions or deletions per human birth too, right (based on the chimpanzee genome finding that indels occur at 1/7th the rate of single-base substitutions)? (Call it 20, as you do above, if you want.) Back in the days before the chimpanzee genome, we used to think that indels occurred about one-tenth as often as single-base substitutions. The chimpanzee comparison showed that we were underestimating the number substantially, so that instead of there being 12 new mutations per person there are actually 17. It's nice to have a more accurate number, but why is 17 utterly absurd when 12 wasn't, and when you're already swallowing 120 other mutations?

"Nearly all of the human insertions are completely covered, whereas only half of the chimpanzee insertions are completely covered. Analysis of the completely covered insertions shows that the vast majority are small (45% of events cover only 1 base pair (bp), 96% are <20 bp and 98.6% are <80 bp), but that the largest few contain most of the sequence (with the approx 70,000 indels larger than 80 bp comprising 73% of the affected base pairs) (Fig. 5). The latter indels >80 bp fall into three categories: (1) about one-quarter are newly inserted transposable elements; (2) more than one-third are due to microsatellite and satellite sequences; (3) and the remainder are assumed to be mostly deletions in the other genome." (Chimpanzee Genome, Nature 2005)

73% are over 70,000 in length. That's my problem Steve. Then when we can look at where they are and how genes are effected we can talk about the a priori assumption of a common ancestor.

Probably because you don't understand what you're reading. I already noted in one post that humans probably have experienced accelerated protein evolution due to accumulating deleterious alleles (the result of a small population size). Did you miss that? I also pointed out that this effect has nothing to do with what you said you were going to do, which was show that the overall rate of indels in humans is too high for known mutation rates.

We are not talking about deleterious alleles, we are talking about 585 genes that are under positive/adaptive selection. Not neutral, not deleterious or even slightly deleterious. I'm talking about gene duplication and the overhaul of the genes involved in the unprecedented expansion of the human brain from that of apes.

Remember, this is about evolution. Where did you think I was going with this?

So tell me, Mark, since you seem to know more about genetics than those of us in the field: how would you go about finding indels using just the complete human genome sequence?

I never said I could find them, I said that the mutation rate changes with the number of base pairs that would have changed increases. Your not going to do this again, face the facts of the overall differences and then lets talk about the differences in the genes.

 

[USincognito]

What it should bring up is a regulatory gene, 118 nucleotides long with 18 substitutions. This regulatory gene is involved in the development of the human cortex. But of course you knew that.

Your response does nothing to address the articles in journals, blogs and the mainstream press which show that HAR1 is evidence for evolution, not the magic bullet you seem to think would kill it for the last year or so.

How about adressing what they have to say rather than appealing to vaguery and incredulity?

First of all, I never said that the article was in error.

Full stop. Where did I ever say you said it was in error? Feel free to quote me if I did, but you're either erecting a straw man or misrepresenting what I've posted.

I have, from the beginning represented your position accuarately - that HAR1 was conserved since our common ancestry with chickens and accellerated since our split with chimps and your objection amounts to "I can't believe it." Please represent my objections to your objection accurately in the future.

I cited and quoted it but it was only recently that I was actually able to obtain the article. For the last 16 months I have been on active duty and I am currently serving in Iraq where the internet is far from reliable.

And I salute you for your service as I have mentioned previously. That doesn't mitigate the fact that your objections to the HAR1 analysis are based on your personal incredulity and not on any scientific grounds.

If you want to call me a liar then don't do it in the third person, tell me right here. I'm not shy about telling a liar what they are to their face. Nature, for instance, lied about the amount of DNA that is the same between the chimpanzee and humans.

I don't toss liar around with the abandon that you do. You are merely confused by the issues that are being discussed (percentage of DNA similiarity), failing to understand certain topics (ERVs) and blinded by your faith position (common ancestry). I don't think you're a liar. You may feel free to call people liars if you want though.

For the umpteenth time, evolutionists will get it right in their peer reviewed publications but other then that I don't trust a word they say.

Telling me it's raining when you're peeing on my leg doesn't make the rain fall no matter how many times you repeat it. You have the original Nature article. You can contact the authors. You have a number of journal articles, blog entries and mainstream press articles explaining how HAR1 is evidence of evolution, not a magic bullet killing it.

How about stepping up to the plate and addressing them rather than wasting CF server space with bluster?