Pete's Quite Thread post

[Tomk80]

I'd like to bridge the current disconnect (which is likely my fault), if possible.

Consider, please, two cases on "equivalent" divergence:
Case A: the divergence between chimpanzee and human genomes was "maximum entropy" (i.e., spread across point mutations only)
Case B: the divergence between chimpanzee and human genomes was "minimum entropy" (i.e., essentially one big substitution [=insertion/deletion])

Now it is clear that the reality as has been observed is somewhere in between these two cases.

But let's (hypothetically, now) imagine Case B. The evidence (in Case B, not in real life) is that a single mutation has caused the evolution represented by the divergence between chimpanzees and humans. How do we respond? Do we say, "sure: an insertion is a mutation, no problem" or do we say "wow! the likelihood of that mutation is infinitessimal [as it represents a 'hopeful monster' type of evolution]".

Ok, now back to reality. I am assuming (yes, assuming: this is NOT a conclusion from the paper, and I have never made such a claim) that, represented in the divergence between chimpanzee and humans there are insertions that are representative of Case B. You folks are saying "sure: an insertion is a mutation, no problem." I am saying "wow! the likelihood of that mutation is infinitessimal [as it represents a 'hopeful monster' type of evolution]"

I recognize that the disconnect might very well be due to the fact that my underlying assumption (that is, that there are Case-B insertions) may be in error. However, we do not yet have the evidence to determine this one way or the other.

What I am still not clear on is why you think that the chance on a large insertion would be infinitessimal, and why it would represent a 'hopeful monster' type of evolution. Why couldn't it be a copy of another part of the genome, or the result of unequal crossing over, or a number of other mechanisms through which large insertions have been hypothesized or observed to occur? I think this is the largest disconnect. You state that mechanisms that we know of could never have caused such large insertions, but I really have no idea why that would be.

 

[jnhofzinser]

Forgive me for skipping the previous post, but this last one highlights our inability to communicate.
"Tom: why do I think the chance...would be infinitessimal?"
I've provided the math that demonstrates that if the only divergence was a big insertion (i.e. case B), the probability is infinitessimal.
"Tom: why couldn't it be a copy?"
Because, by case-B hypothesis, it represents, in its entirety, organism uniqueness. Is it not reasonable to suggest that a copy would not provide that uniqueness?
"Tom: a number of other mechanism..."
Because insertions via known mutative mechanisms tend to be "uninformative". There are exceptions, of course, like retroviral insertions (which, for example, I mistakenly did not consider a "mutation" per se).

The trick is not just to provide a mutative mechanism for large insertions. It would be nice to demonstrate that some specific insertion arose from some specific mechanism. That one is a lot to ask, I understand, and beyond the current technology, so let's either:
- demonstrate that a given mechanism can result in "beneficial" mutations - i.e., contributing to organism uniqueness -or-
- demonstrate that the existing insertions are not "beneficial" - i.e., it doesn't matter.

 

[Tomk80]

Forgive me for skipping the previous post, but this last one highlights our inability to communicate.
"Tom: why do I think the chance...would be infinitessimal?"
I've provided the math that demonstrates that if the only divergence was a big insertion (i.e. case B), the probability is infinitessimal.
"Tom: why couldn't it be a copy?"
Because, by case-B hypothesis, it represents, in its entirety, organism uniqueness. Is it not reasonable to suggest that a copy would not provide that uniqueness?
"Tom: a number of other mechanism..."
Because insertions via known mutative mechanisms tend to be "uninformative". There are exceptions, of course, like retroviral insertions (which, for example, I mistakenly did not consider a "mutation" per se).

The trick is not just to provide a mutative mechanism for large insertions. It would be nice to demonstrate that some specific insertion arose from some specific mechanism. That one is a lot to ask, I understand, and beyond the current technology, so let's either:
- demonstrate that a given mechanism can result in "beneficial" mutations - i.e., contributing to organism uniqueness -or-
- demonstrate that the existing insertions are not "beneficial" - i.e., it doesn't matter.

Okay. I know my previous post is long, but I posted some other questions in that post that may give me more insight in your reasoning here, and might give you more insight in my reasoning. It's still fairly long, but I'll copy it here. You can skip the last question now, I think you have already answered that one in this post (although you can always add for clarification if you think that is necessary of course ):

But I'm still curious as to why you think the mechanisms we know as present that cause insertions and deletions cannot contribute to organisms 'uniqueness'. I'm very much at a loss as how you describe 'uniqueness' and what you think contributes to that 'uniquenss'. I'm also very much at a loss as to what you consider 'new code' and why you think the current mechanisms of insertions that we know cannot account for this.

To give an example. Dogs and wolves differ a lot in their brain structure, both in the brain mass relative to the dog/wolf and in specific structures that are bigger or smaller. Would you describe such a difference as 'uniqueness'? Now, we know that a lot of this difference is especially caused by a differential expression of the genes responsible for different areas of the brain. Would you accept that as a cause for the 'uniqueness'? Now, we know that differential gene expression can either be caused by a duplication of genes (which, interestingly, can sometimes be regulated by the cell itself) or by regulatory sequences of the cell. The lenght of such a regulatory sequence seems to make a difference there, or the space between different regulatory sequences. So an insertion or deletion could in that way have an effect on the expression on the gene, hence contributing to the organisms 'uniqueness'. We know of insertions causing such increases and decreases in regulatory sequences from diseases. Is it then strange to think that we can explain the divergence between organisms, and organisms 'uniqueness' with that mechanism? And what particular reason do we have to think that insertions cannot have accounted for such divergences, other than personal incredulity?

 

[jnhofzinser]

All fair questions -- but they will have to wait, I'm afraid. For now, I will simply say that the difference between dog and wolf (species that can be cross-bred with reproductive offspring) is less significant than the differences between chimpanzee and human. I am quite happy to permit that the mechanisms you describe contribute to wolf/dog uniqueness. Further, I DO think that insertions account for chimp/human uniqueness. But I do NOT think that the insertions in question are the same variety as those that contribute to dog/wolf uniqeness. In particular, the language/thought/consciousness component of human experience (a phenotypic phenomenon with no homology in an ancestor) is not likely to derive from something that simple.

 

[gluadys]

How about a status check -- let me know if I am close...

What I've called "interesting" indels are so very unlikely via mutation that:
- you think they don't exist (you assume that mutation is the default/only? mechanism)
- I think that they must arise via some as-yet-unknown-mechanism (I assume they do exist)

The problem is that you are using "mutation" in two different ways: as a description of a kind of change in the genome, and as a name for the mechanism which brings about this change.

Indel (insertion/deletion) is a description of a kind of change in the genome. So no matter what mechanism causes an insertion or deletion, an indel is always a mutation.

You may or may not be right about some as-yet-unknown mechanism that causes an indel, but the indel is still a mutation (=a change in the genome) whatever the mechanism that caused it.

In short, in relation to the genome, mutation is a description, not a causal factor. It is in relation to the function of a gene that mutations are causal factors.

 

[mark kennedy]

All fair questions -- but they will have to wait, I'm afraid. For now, I will simply say that the difference between dog and wolf (species that can be cross-bred with reproductive offspring) is less significant than the differences between chimpanzee and human. I am quite happy to permit that the mechanisms you describe contribute to wolf/dog uniqueness. Further, I DO think that insertions account for chimp/human uniqueness. But I do NOT think that the insertions in question are the same variety as those that contribute to dog/wolf uniqeness. In particular, the language/thought/consciousness component of human experience (a phenotypic phenomenon with no homology in an ancestor) is not likely to derive from something that simple.

I don't mean to interrupt but this is one of the main issues I am concerned with. For canines to diverge from somekind of a wild wolf to a domesticated dog would not require any signifigant changes in the genome. What is particularly important is that the effective genome is very intolerant of changes like insertions and deletions.

The differences between the chimpanzee and human genomes have been indentified in part as indels (insertions/deletions) but this is based on the presumption of common ancestory. When you have two strings of DNA being compared in strings that span some 42 million nucleotides where they don't line up is treated as if it where the result of accumulated mutations. Since common ancestory is no longer questioned the foregone conclusion is that these are changes that have happened over roughly 10 million years. I think these differences indicate seperate lineage since there are limits to the number of changes the effective genome can endure.

 

[Manic Depressive Mouse]

I'll take your lack of explaination on the multitude of human species we know to have existed as an admission that your claim "humans do not speciate" is an assertion you cannot back up, Mark.

 

[mark kennedy]

I honestly don't understand what is so hard to grasp about this but if you look at the shear number of changes that would be required for humans (homo sapeins) to have diverged from a common ancestor of the chimp it is just an extraordinary level of changes.

Human Chromosome 21 is about 42,000,000bps long, when compared to the Chimpanzee chromosome 22 they noted 5% of the differences were indels and another 1.44% single base substitutions. You take 42,000,000 and multiply it by 6.44% and you get 2,704,800 bps. What is even more supprising is that percentage wise there are more in the effective genome then other regions.

With 6.4 x 109 base pairs in the diploid genome, a mutation rate of 10^-8 means that a zygote has 64 new mutations. It is hard to image that so many new deleterious mutations each generation is compatible with life, even with an efficient mechanism for mutation removal. Thus, the great majority of mutations in the noncoding DNA must be neutral.

This particular rate is based on "per genome per sexual generation", estimated rate. That means that the overall mutations in a single chromosome will be lower still. How is it even conceivable that this creates no problem for evolution? I don't have an exact number of indels in the protein coding genes but when they are talking about 20% that is an enormous number of changes becoming fixed throughout the entire species no matter how much time you think you have to work with.

When you look at all of the other influnces that have created speciation like eastern/western gorillas, chimps/bonobos humans have been subject to the same forces and there still only one branch of the homo sapein line. Genetic drift, geologic isolation, mutations etc are supposed to be what drives evolution but the human race would seem to be uniquely immune to these influences. Instead we are seeing more differences within races (dems) then we see between them.

Why do they not have a beneficial mutation rate for humans? Because the effects observed, demonstrated and discussed in human effective genomes were; Apert's Syndrome, multiple endocrine neoplasia type B (MEN2B), and type A (MEN2A). There is no such thing as a human beneficial mutation rate just rare postitive effects that are seen in small minorities with marginal effects. If this is all that evolutionary biology has for a demonstrated mechanism then they have no genetic basis for humans evolving from apes. It's not a theory, it's not even a good hypothesis, its a myth.

Just one more thing, equating the theory of evolution with the single common ancestory is bogus head games. Equating evolution in turn with science and the only other alternative, divine providence, is equally bogus. No other field of science would be allowed to get away with this but evolutionary biology is and that is what makes this whole issue so utterly ridiculas.

 

[Valkhorn]

Just one more thing, equating the theory of evolution with the single common ancestory is bogus head games. Equating evolution in turn with science and the only other alternative, divine providence, is equally bogus. No other field of science would be allowed to get away with this but evolutionary biology is and that is what makes this whole issue so utterly ridiculas.

So in other news you rabbit on for three paragraphs about nothing - showing that you really don't understant evolution, then in the final paragraph, in a stunning array of wit and foresight, make a bogus claim which you do not substantiate.

You simply cannot see the forest for the trees, mister.

 

[yossarian]

I honestly don't understand what is so hard to grasp about this but if you look at the shear number of changes that would be required for humans (homo sapeins) to have diverged from a common ancestor of the chimp it is just an extraordinary level of changes.

why is it extraodinary?

calculations please

There is no such thing as a human beneficial mutation rate just rare postitive effects that are seen in small minorities with marginal effects. If this is all that evolutionary biology has for a demonstrated mechanism then they have no genetic basis for humans evolving from apes. It's not a theory, it's not even a good hypothesis, its a myth.

how would you go about screening for beneficial mutations mark?

we just keep going around and around, because you can't answer simple questions. All you really have for an argument is personal incredulity

 

[mark kennedy]

why is it extraodinary?

calculations please

I did and you simply respond with pedantic one liners that ignore them.

how would you go about screening for beneficial mutations mark?

It does not require some new standard of screening, they know a beneficial effect when they see it. There have been beneficial mutations observed and demonstrated but assuming millions of them being fixed in functionally important genes is just plain ridiculas.

we just keep going around and around, because you can't answer simple questions. All you really have for an argument is personal incredulity
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Simple isn't the word I would use, I would describe them a pedantic circular statements rather then an honest inquiry into the scientific basis. I did quote directly from the spontaneous mutation rate paper and the technical details have been laid out for you. For whatever reason you would rather talk in circles around the actuall facts and make glib personal insinuations.

The paper makes explicit calculations of the mutation rates in humans and guess what, they did not bother to discuss a single beneficial effect in their section on homo sapeins, why do you think that is?

 

[mark kennedy]

So in other news you rabbit on for three paragraphs about nothing - showing that you really don't understant evolution, then in the final paragraph, in a stunning array of wit and foresight, make a bogus claim which you do not substantiate.

You simply cannot see the forest for the trees, mister.

I did go into the substantive issues; the mutation rate for homo sapeins and the differences between human and chimpanzee DNA but of course that is ignored. I have substantiated that the differences between chimpanzees and humans cannot be accounted for by spontaneous mutations with one irrefutable premise. The deleterious effect of mutations that effect the development of vital organs are the only effect ever observed or demonstrated.

I understand evolution perfectly well, it does not need the single common ancestor model and never did. All single common ancestory does is eliminate theistic reasoning from evolutionary biology and it has no genetic basis in this crucial line of descent of homo sapeins from apes. Sure my statements are very general, I don't have time to accumulate technical details that are simply ignored and responded to with pedantic satire.

 

[gluadys]

The deleterious effect of mutations that effect the development of vital organs are the only effect ever observed or demonstrated.

Actually, I am still waiting for your account of how this affects the evolution of species.

 

[Pete Harcoff]

There have been beneficial mutations observed and demonstrated but assuming millions of them being fixed in functionally important genes is just plain ridiculas.

Millions?

Do tell, mark, where are you getting this from? Exactly how many beneficial mutations does it take to make a human?

 

[mark kennedy]

Millions?

Do tell, mark, where are you getting this from? Exactly how many beneficial mutations does it take to make a human?

You tell me Pete, what is 6.44% of 42 million? Mind you, that is in one chromosome and the mutation rate you are using is genome wide. There is also the problem of the unavoidable deleterious and neutral mutations that would have vastly outnumbered them. What is more there are the marginal effects of what you would characterize as a beneficial effect that would produce an evolutionary change.

I will be honest with you, I think I know the answers to some of the points I am making. Things like gene duplication, retrotranspostions and various other things that go on at a genetic level. The paper that you are baseing your calculations on did not have a beneficial mutation rate and there is a simple explanation for that. They couldn't find enough beneficial effects from mutations to base them on.

 

[mark kennedy]

Actually, I am still waiting for your account of how this affects the evolution of species.

I am still waiting you to account for the changes that led to the expansion of the human brain from on the size of the chimpanzee.

 

[Pete Harcoff]

You tell me Pete, what is 6.44% of 42 million? Mind you, that is in one chromosome and the mutation rate you are using is genome wide. There is also the problem of the unavoidable deleterious and neutral mutations that would have vastly outnumbered them. What is more there are the marginal effects of what you would characterize as a beneficial effect that would produce an evolutionary change.

Some questions:

Do you think that every single mutation that was fixed in the human genome must have been beneficial? Even including the mutations in non-coding DNA?

And do you think that every single nucleotide that is different requires a beneficial mutation all its own?

 

[Pete Harcoff]

Actually, I am still waiting for your account of how this affects the evolution of species.

I think it's safe to say that mark will never answer this. Why, I'm not sure, as it can't be too hard to crunch some numbers based on deleterious mutation rates.

 

[mark kennedy]

I think it's safe to say that mark will never answer this. Why, I'm not sure, as it can't be too hard to crunch some numbers based on deleterious mutation rates.

I think it is fair to say that you will never admit what 6.44% of 42 million is and how it got there.

 

[mark kennedy]

Some questions:

Oh, I like this part..

Do you think that every single mutation that was fixed in the human genome must have been beneficial? Even including the mutations in non-coding DNA?

I think in order for a mutation or any change to be fixed in the genome there would have to be a species wide event that excluded none of the descendants.

And do you think that every single nucleotide that is different requires a beneficial mutation all its own?

In the effective genome, absolutely! It's called the physiological cost of adaptation and if it costs more then it benefits it is eliminated by the force of natural selection. Some times I think creationists are doing themselves a diservice by opposing natural selection, the crucial line of proof is found in the costs of adaptive evolution.

A couple of questions for you Pete:

What does one beneficial effect from a mutation cost in deleterious effects?

What is the proportion of neutral effects as compared to deleterious and neutral effects?