Humans DNA is 99% similar to that of chimps?

[mark kennedy]

Mark's access to TEH INTERWEBS is limited. He's deployed (in Iraq) and he can't get online every day.

Actually, I am training here a Camp Atterbury, Indiana for duty in Iraq. The training schedule is pretty demanding so I get in here when I can. I won't actually be in Iraq till sometime in September.

Grace and peace,
Mark

 

[mark kennedy]

No, if the divergence for single-base substitutions were 10% I would be surprised. That is, if otherwise similar stretches of DNA differed by 10% of their bases, or if there were 300 million single-base differences between the two genomes, I would have been very surprised.

Ok, I was just wondering where the line is drawn, thanks for clarifying.

No, it says that 585 genes show KA/KI > 1, and that 585 is 4.4% of 13,454, the total number of genes examined.

I thought it was something like that but these things are so meticulasly worded it's sometimes hard to follow.

The list of individual genes is available as online supplementary information. I could put a copy on the web if you want.

I would appreciate that since I am having some trouble following the Hapmap pages.

No, that's not a very good estimate. Say 50-70 mutations per genome copy per generation, or 100 or so per individual (since we all have two copies of the genome). About 1.5% of the genome codes for amino acids, so expect 1.5 - 2.0 mutations in coding sequence per person, of which 1.0 - 1.3 will change an amino acid. Of these, 3/4ths are deleterious. So I expect an average of ~0.75-1.0 deleterious coding mutations per person per generation.

What has me puzzled, let's say you have 4 mutations in the coding sequence and natural selection eliminates 3 of them. The remaining mutation, maybe just a single codon, is still being passed on to further generations. Is it conceivable that over time the original sequence can be recovered somehow? I only ask because I heard of a mustard plant experiment where they deliberatly mutated a population of plants. Keeping them totally isolated 1/10 returned to the grandparent form.

As far as I can tell, the NCBI web page is wrong, or perhaps based on a very early, crude estimate. If you look at the NCBI browser for the chimp genome, you'll find that they actually give the total length as 3,084.3 Mb. Similarly, the UCSD genome browser gives 3,083,992,161 bases (using the same genome assembly, I believe), and the same browser gives the length of the human genome as 3,076,889,702 bases, a difference of 0.23%. (I also checked with one of the chimp genome sequence experts, who confirmed that there is no evidence for one genome being significantly larger than the other.)

Ok, I was having trouble finding a specific number and then I stumbled onto the number I posted. My real interest in the browser is the hope that I will eventually be able to see the comparisions of specific genes. The UCSD pages are pretty confusing, I prefer the simplicity of the ORNL pages. It's a little more on my level if I can fight the temptation to wonder of on the various tangents I find there.

I don't know what you mean here. The mutation rate we're talking about is in the germ line, so these are permanent changes that are passed down to all descendents. Most of the changes will not become fixed in the population, true, but the relevant number for the population is the total number of mutations occuring in the population, which is ~100 x 6 billion individuals.

I'm just under the impression that not all germline mutations are cumulative. Lets say we have 130 mutations passed on to one gereration, since they are in the germline they are inheritable. If, for instance, they are the result of a transcript error then it seems there would be a way for the error to be corrected. The real issue here is what causes an adaptative trait, the growth of the human brain in the Homo lineage being my central focus. I dare say that randomly occuring mutations are much of an explanation for this. Even if the common ancestory of men and apes is an actual fact, there has to be a better genetic mechanism for this then random mutations.

6 million years, plus or minus 2 million.

Now don't get worked up over this, I am just trying to get a handle on the concept here. 130 per generation would be 65,000,000 over a 10,000,000 Mya period. I'm a little dense as you are no doubt becoming painfully aware but this doesn't add up for me.

The mutation rate you've been given before. Appoximately 2x10^-8/bp/generation in each copy of the genome for single base substitutions, and ~0.3x10^-8/bp/generation for indels. The fixation rate during most of the human lineage has been equal to the mutation rate for a single genome copy. During the last few thousand years, the fixation rate has dropped way off, since mutations are now accumulating as variants, rather than fixing (due to the large population size).

Brother, if it had been anyone but you who said that I would think this was guess work. However, I expect you have an understanding of how the dynamics change with population size, I am still a little confused. It seems to me that if our ape ancestors accumulated such dramatic adaptive changes in populations within the tens of thousands. The modern Homo sapien would be producing changes that were exponentially higher and thus creating vast diversity. You seem to be saying that our genome has stabalized because of the population being so large, that's the opposite of what I would have thought.

~120 million base pairs, not including inversions.

I was thinking 35 Mb + 90 Mb = 125 but clearly those are round numbers. The 9 pericentric inversions mentioned in the paper refered to the larger inversions which added up to 20 Mb some 2-4 Mb long.

A single genetic estimate is in conflict. Since the genetic estimate in question used mtDNA over a very long time period (the calibration point was not a primate, remember), it has a very large uncertainty. Contrary to your previous statement, mtDNA is just about the worst molecular clock system to use for long time periods. It has sites that mutate at wildly different rates, and as you move to longer and longer periods, more of them saturate, skewing the result. If you recall, the paper you quoted the mtDNA results from listed a range of genetic estimates for the human/chimp split time from something like 2.5 million years to 13 million years. Why are you focusing on the extreme value from the range, especially since the measurement is suspect?

You allready told me what I was most concerned about, whether or not mtdna was considered a molecular clock. It was the fact that the genetic estimates were so inconsistant that got my attention so I just picked a choice quote. Given what you are telling me about mtDNA I think we need not worry about it giving us a reliable timeline which is what I'm really looking for.

I have another question if you have the patience for it. Could you kindly tell me what this means?

"Although most (66%) of the autosomal base pairs (bp) duplicated in humans are shared between human and chimpanzee (Table 1), a surprisingly large fraction (33% or 26.5 out of 79.8 Mb) is duplicated in human but not chimpanzee (Table 1)."

http://www.nature.com/nature/journal/v437/n7055/full/nature04000.html

Are they talking about disease traits that are not shared by humans and chimpanzees. It's no big deal but it kind of threw me.

I really don't have as much time as I would like to have for this. I want to get better at using those chomosome browsers to get a better look at how the actual genes diverge. It probably wouldn't hurt me any to take some kind of a genetics class when I get back from the sandbox.

Grace and peace,
Mark

 

[Robert the Pilegrim]

Actually, I am training here a Camp Atterbury, Indiana for duty in Iraq. The training schedule is pretty demanding so I get in here when I can. I won't actually be in Iraq till sometime in September.

Grace and peace,
Mark

May God go with you,
Robert the Pilegrim

 

[shernren]

Brother, if it had been anyone but you who said that I would think this was guess work. However, I expect you have an understanding of how the dynamics change with population size, I am still a little confused. It seems to me that if our ape ancestors accumulated such dramatic adaptive changes in populations within the tens of thousands. The modern Homo sapien would be producing changes that were exponentially higher and thus creating vast diversity. You seem to be saying that our genome has stabalized because of the population being so large, that's the opposite of what I would have thought.

Remember that a mutation "spreads" through a population by reproduction. Imagine being in a time where the only type of iris color is brown, and all of a sudden a man gets a mutation which confers a green iris, which is passed along his germline. The only way this green-iris mutation "spreads" is when the man (or his descendants) give birth to a green-eyed monster while at the same time someone brown-eyed dies: in effect, the green-eye person replacing the brown-eyed person.

Let's say this man is living in a population of 10,000, and let's assume that birth rate is equal to death rate (so that the population is constant). Every time someone is born with green eyes and someone with brown eyes dies, the proportion of green-eye rises. How long will it take for the green-eye gene to reach 50%? It will take 5,000 "substitutions".

On the other hand, let's say he is living as the sole green-eye-guy on a planet with 6 billion brown-eyed humans. How long will it take for the green-eye gene to reach 50%? We need 3 billion "substitutions": this guy eventually needs 3 billion green-eyed progeny before the gene can reach 50%.

Whatever the effect of the mutation (advantageous, neutral, or deleterious) you can see that mutations take longer to spread in a larger population because when the population is big, it takes more time for their relative frequency to increase. If the mutation is advantageous, then the speed of fixation will increase because more offspring are being born with the advantageous trait than without; if deleterious, the mutation will slowly be driven to "extinction". But the basic principle is same throughout.

At least, that's what I understand of the genetic drift mechanisms.

 

[Smidlee]

What everyone seems to overlook is that the brain and the liver would have had to undergo dramatic changes. Evolutionists want to compare this to sickle-cell or other supposed beneficial mutations but there has never been one single beneficial effect from a mutation affecting the human brain. Mutations create brain tumors not imporved fittness, no such thing exists in natural science but they still want you to believe its a scientific fact.

And while the brain (liver) was going though those serious changes all those pseudogenes we have in common with chimps and other apes remain unchanged for millions of years. Pseudogenes which claimed to have no funtion is where NS+RM is suppose to do it work.
Does it make sense that our brain went though some major changes, which as you point out a mutations in this area can lead to serious defects, while those useless pseudogenes lefted untouched for millions of years?
It seems like another case of supernatural selection to me.
"Superman (mutition and national selection) Returns" is now in theaters.

 

[sfs]

I would appreciate that since I am having some trouble following the Hapmap pages.

Human/chimp gene-by-gene comparisons:
http://www.broad.mit.edu/personal/sfs/chimp-s6.xls

What has me puzzled, let's say you have 4 mutations in the coding sequence and natural selection eliminates 3 of them. The remaining mutation, maybe just a single codon, is still being passed on to further generations. Is it conceivable that over time the original sequence can be recovered somehow? I only ask because I heard of a mustard plant experiment where they deliberatly mutated a population of plants. Keeping them totally isolated 1/10 returned to the grandparent form.

That was a decidedly odd result. If correct (which is always a big if, with novel and surprising results), it implies a completely unknown mechanism for recovering previous versions of a gene. If such a thing does exist, it doesn't seem to function very often, since that kind of reversion could have been seen in lots of genetics experiments and hasn't been.

I'm just under the impression that not all germline mutations are cumulative. Lets say we have 130 mutations passed on to one gereration, since they are in the germline they are inheritable. If, for instance, they are the result of a transcript error then it seems there would be a way for the error to be corrected. The real issue here is what causes an adaptative trait, the growth of the human brain in the Homo lineage being my central focus.

That may be the real issue that you're most interested, but the real issue I'm addressing is your repeated claim that the rate of single-base substitutions and the rate of indels between humans and chimps, given the known mutation rate, represents some kind of problem for common descent. You have yet to present any evidence for this claim.

Now don't get worked up over this, I am just trying to get a handle on the concept here. 130 per generation would be 65,000,000 over a 10,000,000 Mya period. I'm a little dense as you are no doubt becoming painfully aware but this doesn't add up for me.

By 130 per generation I assume you mean mutations. That's in the right ballpark for the number of mutations per person; the number of mutations per genome copy is half that, giving you 32,000,000 over a 10 My period. That should be compared with the observed number of mutational differences, which was 40,000,000. Given the crudity of the estimates, quite a good agreement.

Brother, if it had been anyone but you who said that I would think this was guess work. However, I expect you have an understanding of how the dynamics change with population size, I am still a little confused. It seems to me that if our ape ancestors accumulated such dramatic adaptive changes in populations within the tens of thousands. The modern Homo sapien would be producing changes that were exponentially higher and thus creating vast diversity. You seem to be saying that our genome has stabalized because of the population being so large, that's the opposite of what I would have thought.

I'm not sure what you're asking here. A large population (as in modern humans) makes fixation of new neutral mutations much less likely. Fixation of beneficial alleles, on the other hand, will increase in a large population: each beneficial allele will take longer to fix, but there will be many more of them in a large population, both since there are more individuals to mutate and because alleles with only small beneficial effects can be affected by selection in a large population.

I have another question if you have the patience for it. Could you kindly tell me what this means?

"Although most (66%) of the autosomal base pairs (bp) duplicated in humans are shared between human and chimpanzee (Table 1), a surprisingly large fraction (33% or 26.5 out of 79.8 Mb) is duplicated in human but not chimpanzee (Table 1)."

http://www.nature.com/nature/journal/v437/n7055/full/nature04000.html

I'm not sure what the basis for "surprise" is, but what they're talking about are places in the human genome that are duplicated elsewhere in the human genome, i.e. two or more long stretches of nearly identical DNA. Of such regions in humans, 66% are also found as duplicates in the chimp genome, suggesting that the duplication predated the human/chimpanzee split. The other third are found only in humans, suggesting that they occurred since the split.

 

[mark kennedy]

Human/chimp gene-by-gene comparisons:
http://www.broad.mit.edu/personal/sfs/chimp-s6.xls

I have tried a couple of times to get a look at this but I'm not having any luck. There is something about the firewall on these computers that won't let me. I'll hang onto the address and keep trying.

That was a decidedly odd result. If correct (which is always a big if, with novel and surprising results), it implies a completely unknown mechanism for recovering previous versions of a gene. If such a thing does exist, it doesn't seem to function very often, since that kind of reversion could have been seen in lots of genetics experiments and hasn't been.

The researchers seemed to be at a loss for an explanation but it was a fascinating little puzzle for them I'm sure.

http://www.npr.org/templates/story/story.php?storyId=4561167

I believe that's the interview on NPR if your interested in getting some of the discussion.

That may be the real issue that you're most interested, but the real issue I'm addressing is your repeated claim that the rate of single-base substitutions and the rate of indels between humans and chimps, given the known mutation rate, represents some kind of problem for common descent. You have yet to present any evidence for this claim.

That's what has me puzzled about you in particular and evolutionary theory in general. We are talking about well over a 100 million nucleotides being altered on a macro scale. The evidence is right in front of you, the diversity itself and the timeframe with which they had to occur. The genes affecting the brain and liver do not respond well to alterations (mutations) but they would have had to change some things dramatically. Obviously, there are a lot of factors to consider but frankly the idea of spontaneous mutations pulling this off is just to far fetched.

By 130 per generation I assume you mean mutations. That's in the right ballpark for the number of mutations per person; the number of mutations per genome copy is half that, giving you 32,000,000 over a 10 My period. That should be compared with the observed number of mutational differences, which was 40,000,000. Given the crudity of the estimates, quite a good agreement.

130 germline mutations per generation in roughly a 5 million year timeframe. The SNPs come to 32 Mb as we are both well aware but the indels come to about 90 Mb, 130 per generation comes to about 32 Mb which could account for the SNPs. 32 Mb in 10,000,000 years is not 125 Mb in 5-7 Mya. With all due respect Steve, what about all those indels and inversions?

I'm not sure what you're asking here. A large population (as in modern humans) makes fixation of new neutral mutations much less likely. Fixation of beneficial alleles, on the other hand, will increase in a large population: each beneficial allele will take longer to fix, but there will be many more of them in a large population, both since there are more individuals to mutate and because alleles with only small beneficial effects can be affected by selection in a large population.

I realize that there are beneficial alleles to be had and obviously, they would have greater longevity in the population. What is giving me reason for pause is that what I am seeing is a very marginal variation in the genetic code of human populations worldwide. Unless I am mistaken beneficial alleles are not totally reliant on mutations, in fact I have long believed that most adaptation comes from recombinations of existing genes.

It would have only been in relativly recent natural history (tens of thousands of years) that human populations were approaching billions of people. I don't know what the populations of early human ancestors was but it would have been in the tens of thousands. It seems odd that major evolutionary changes are going on in smaller populations but far less likely in the huge populations of modern human beings.

I'm not sure what the basis for "surprise" is, but what they're talking about are places in the human genome that are duplicated elsewhere in the human genome, i.e. two or more long stretches of nearly identical DNA. Of such regions in humans, 66% are also found as duplicates in the chimp genome, suggesting that the duplication predated the human/chimpanzee split. The other third are found only in humans, suggesting that they occurred since the split.

I wasn't supprised, I was just not getting what they were saying. I was just looking for clarification.

I'll get to the gene to gene comparisons at my first opportunity. I do appreciate you posting those and I'll let you know what I come up with when I can get a look at them.

Grace and peace,
Mark

 

[Assyrian]

Human/chimp gene-by-gene comparisons:
[URL="http://www.broad.mit.edu/personal/sfs/chimp-s6.xls"]http://www.broad.mit.edu/personal/sfs/chimp-s6.xls[/URL]

I have tried a couple of times to get a look at this but I'm not having any luck. There is something about the firewall on these computers that won't let me. I'll hang onto the address and keep trying.

I wasn't able to open it by clicking on the link either. Try downloading the file and open it from your desktop. That seems to work.

 

[rmwilliamsll]

I wasn't able to open it by clicking on the link either. Try downloading the file and open it from your desktop. That seems to work.

just as a useful aside.
look at the extension, it is a microsoft excel file.
you must have a helper function installed on your browser that knows how to open this type of file.
see your browser's online help page.
when you download it, your operating system needs to know how to open that type of file, when you try to open it.
if you are running a microsoft product and have office or excel installed then you will open it successfully.
google excel file reader if you don't and need to read xls files.
same type of reasoning applies to any files types not registered or known by your browser.

 

[sfs]

That's what has me puzzled about you in particular and evolutionary theory in general. We are talking about well over a 100 million nucleotides being altered on a macro scale.

As I've pointed out to you repeatedly, ~100 million altered nucleotides is what evolutionary theory would have predicted. Yet you continue to claim that this number somehow presents a problem for evolutionary theory. Could you please state what the problem is?

The evidence is right in front of you, the diversity itself and the timeframe with which they had to occur. The genes affecting the brain and liver do not respond well to alterations (mutations) but they would have had to change some things dramatically. Obviously, there are a lot of factors to consider but frankly the idea of spontaneous mutations pulling this off is just to far fetched.

I'm sorry, but "seems far-fetched to Mark Kennedy" is a not a useful scientific criterion for rejecting a hypothesis. You have to formulate an argument for the changes being too large, and you haven't done so, despite many posts on the subject

130 germline mutations per generation in roughly a 5 million year timeframe. The SNPs come to 32 Mb as we are both well aware but the indels come to about 90 Mb, 130 per generation comes to about 32 Mb which could account for the SNPs. 32 Mb in 10,000,000 years is not 125 Mb in 5-7 Mya. With all due respect Steve, what about all those indels and inversions?

With all due respect, what about all those indels and inversions? What is the problem with them? The 80 or 90 Mb of indels are spread out over 5 million insertion and deletion events. So what? Why am I supposed to be impressed by that number?

I realize that there are beneficial alleles to be had and obviously, they would have greater longevity in the population. What is giving me reason for pause is that what I am seeing is a very marginal variation in the genetic code of human populations worldwide.

Variation between individual humans is almost one tenth of the the difference between humans and chimpanzees, and yet you consider the former negligible and the latter enormous. Why? Humans and chimpanzees have been accumulating differences between them for ten times as long as humans have been accumulating differences between each other, so why is it surprising that there are ten times as many differences?

It would have only been in relativly recent natural history (tens of thousands of years) that human populations were approaching billions of people. I don't know what the populations of early human ancestors was but it would have been in the tens of thousands. It seems odd that major evolutionary changes are going on in smaller populations but far less likely in the huge populations of modern human beings.

Observable change happens at different rates under different conditions. It's a moot point anyway, since we have no idea how fast humans have been changing in the last few thousand years -- that's just too short a time period to see morphological change (except under extreme circumstances).

I wasn't supprised, I was just not getting what they were saying. I was just looking for clarification.

The authors were the ones who expressed surprise, not you. I still don't see why.

 

[mark kennedy]

"Darwin wanted to establish... that the species — including human beings — were created by, and evolve according to, processes that are entirely natural, chance-generated, and blind." (Louis Menand)

As I've pointed out to you repeatedly, ~100 million altered nucleotides is what evolutionary theory would have predicted. Yet you continue to claim that this number somehow presents a problem for evolutionary theory. Could you please state what the problem is?

The problem is that you account for the SNPs...

By 130 per generation I assume you mean mutations. That's in the right ballpark for the number of mutations per person; the number of mutations per genome copy is half that, giving you 32,000,000 over a 10 My period. That should be compared with the observed number of mutational differences, which was 40,000,000. Given the crudity of the estimates, quite a good agreement.

But you haven't got much to say about the indels that are 90 Mbs. What is more an inversion of 4 Mb would be an astronomical alteration of the nucleotide sequence, tell me Steve, did it all happen at once or offer successive generations? SNPs are covered in your discussion but were did all these indels come from?

Now I realize that the nucleotide sequence doesn't really tell us a whole lot, but one thing is certain, the differences are considerably more then we have been told.

"DNA sequences are approximately 1.2% divergent (based on substitutions) from those of their nearest genetic relative, the chimpanzee, 1.6% from gorillas, and 6.6% from baboons"

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

This is presented as an actual fact and clearly it is not. We are not divergant from chimpanzees by 1.2% but at least 4% when you count the indels. Why doesn't anyone want to count or account for the indels?

I'm sorry, but "seems far-fetched to Mark Kennedy" is a not a useful scientific criterion for rejecting a hypothesis. You have to formulate an argument for the changes being too large, and you haven't done so, despite many posts on the subject

The key is mutations of DNA changes that accumulate over time. Those germline mutations (130) are not cumulative but cyclical like most evolutionary trends. Even if everyone of them was accumulated and that is 65 Mbs over a 6 Mya period. The Chimpanzee Genome Consortium identified 125 Mb of SNP/indel differences in the nucleotide sequences. Correct me if I'm wrong, that leaves over half of them unaccounted for, even if you assume that all the germline mutations are cumulative.

The question remains:

With all due respect, what about all those indels and inversions? What is the problem with them? The 80 or 90 Mb of indels are spread out over 5 million insertion and deletion events. So what? Why am I supposed to be impressed by that number?

Wouldn't you be impressed if a human population was passing on 400 germline mutations per generation. I think I would be checking the area for radiation or some kind of a chemical in the water because it does not normally happen. If it did there would be terrible disease and disorders.

Variation between individual humans is almost one tenth of the the difference between humans and chimpanzees, and yet you consider the former negligible and the latter enormous. Why? Humans and chimpanzees have been accumulating differences between them for ten times as long as humans have been accumulating differences between each other, so why is it surprising that there are ten times as many differences?

Ok, humans diverge by .1% and diverge from chimpanzees by at least 4%. Which means that that varitation between humans and chimpanzees is more like 40 times what it is between humans. For one thing, if the divergance between humans and chimps was was 1/10 of what it is between humans the divergance between humans and chimps would be 1%. Clearly they are not and I think you are very well aware of that fact. In order to get this level of divergance (3%) would take a fixation of randomly occuring mutations that average of >400 fixed in the population. That is in addition to the fact that they would have had to be cumulative and you act as if I have no evidence that causes a problem for common descent?

Do you
1) not understand that I'm saying that mutations must accumulate at a rate of >400 bs per generation?
2) not believe it when we say it?
3) forget it?
4) not care?
5) something else I can't think of?

Observable change happens at different rates under different conditions. It's a moot point anyway, since we have no idea how fast humans have been changing in the last few thousand years -- that's just too short a time period to see morphological change (except under extreme circumstances).

The timeframe may not be that long but with populations in the billions the level of divergance should be much higher if they are cumulative. None of the mechanisms that create speciation events are relavant to human evolution, we have been subject to all of them and still interbreed at random. There are Eastern and Western African Gorillas, Chimpanzees and Bonobos. There is one species of Homo sapien and we do not speciate because we cannot speciate. Before we get to the gene to gene comparisons I wanted to post some quotes and see what, if any response to them you might have.

"The large number of amino acid substitutions suggests a high rate of adaptive evolution in primates. The expected number of amino acid substitutions is 2382 (4151 x 70/122) based on the A/S ratio of common polymorphism and the excess is 1278. Therefore, a large proportion, 35%, of amino acid substitutions between humans and old world monkeys are estimated to have been driven by positive selection. Extrapolating this proportion to the total amount of coding DNA in the genome (5 x 107 bp) yields an estimate of up to 1 advantageous substitution every 200 years since humans separated from old world monkeys 30 million years ago. (More Precise Expressions for the Cost of Natural Selection, Nature 1960)

Consider that population geneticists typically estimate that only 1 in 50 beneficial mutations have a chance to even reach fixation15. This problem is aggravated by the fact that a cost must be incurred to spread any new trait through the population (those without the trait must eventually die off). The famous geneticist J.B.S. Haldane showed that under favorable assumptions only one new, beneficial substitution could be completely substituted in a population every 300 generations. So in 10 million years, twice the time since the alleged chimp/human split from a common ancestor, only 1667 beneficial substitutions could occur.

http://www.evolutionfairytale.com/articles_debates/mutation_rate.htm

The authors were the ones who expressed surprise, not you. I still don't see why.

I just wasn't sure I understood the statement, that's all.

So far as I can tell the SNPs can be accounted for if you assume the germline mutations occuring naturally are cumulative. The indels are of no interest since they were rarely mentioned in mainstream evolutionary discussions about the molecular differences between humans and chimpanzees. Finally, if the percentage of the level of divergance is slight (a mere 4%) then it doesn't matter what the substitution rate would have had to be.

I don't know why you keep calling for an argument when the evidence speaks for itself. That is the best part of an ad hominid approach to evidencial apologetics, no one is arguing to the contrary.

Grace and peace,
Mark

 

[sfs]

But you haven't got much to say about the indels that are 90 Mbs.

The indels are 5 million mutation events, implying a mutation rate seven times smaller than the single-base mutation rate. Remember, your claim is that the number of indels is too large to be accounted for by the mutation rate. Could you please support that claim?

What is more an inversion of 4 Mb would be an astronomical alteration of the nucleotide sequence

Inversions, whether large or small, may have no effect at all on the organism. If a gene and all its regulatory sequences are inverted together, it will function in the same way in the inverted sequence as in the original sequence -- the cell's machinary reads in both directions. Many inversions will be deleterious, of course, and these will be removed by natural selection.

As I've pointed out to you previously, there is a single inversion of almost 1 million base pairs that is polymorphic in contemporary humans, and it produces little or no effect on those who have it. (There is a suggestion that it actually increases fecundity.) This is not the only inversion known in humans. So 20 Mb in inversions between humans and chimpanzees is not surprising.

, tell me Steve, did it all happen at once or offer successive generations? SNPs are covered in your discussion but were did all these indels come from?

Each inversion and each insertion or deletion, and each single-base substitution (they're not SNPs) occurred in a particular generation and then spread through the population. Just as each inversion and each insertion or deletion and each single-base substitution that is polymorphic in the modern population occurred in a particular generation and then spread (to the whatever extent) through the population.

Now I realize that the nucleotide sequence doesn't really tell us a whole lot, but one thing is certain, the differences are considerably more then we have been told.

"DNA sequences are approximately 1.2% divergent (based on substitutions) from those of their nearest genetic relative, the chimpanzee, 1.6% from gorillas, and 6.6% from baboons"

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

This is presented as an actual fact and clearly it is not. We are not divergant from chimpanzees by 1.2% but at least 4% when you count the indels.

Mark, read what you just quoted. "DNA sequences are approximately 1.2% divergent (based on substitutions) from those of their nearest genetic relative, the chimpanzee." Based on substitutions means they're not counting the indels, just the substitutions. It's not the only way of measuring genetic differences, but it's a perfectly valid one, and the one for which we have the best measurements. Your point here is simply wrong.

Why doesn't anyone want to count or account for the indels?

Because they're harder to identify, and scientists tend to focus on things they can measure. Also because there are fewer of them, they tend to be less relevant to function, and it's easier to make mistakes when measuring them.

The key is mutations of DNA changes that accumulate over time. Those germline mutations (130) are not cumulative but cyclical like most evolutionary trends.

Germline mutations are cumulative, at least in the vast majority of cases. I don't know what you mean by cyclical here.

Even if everyone of them was accumulated and that is 65 Mbs over a 6 Mya period.

You are again confusing the number of mutations with the number of base pairs that change in the mutation. An insertion of 1 million base pairs is a single mutation.

The Chimpanzee Genome Consortium identified 125 Mb of SNP/indel differences in the nucleotide sequences. Correct me if I'm wrong, that leaves over half of them unaccounted for, even if you assume that all the germline mutations are cumulative.

Yes, you're wrong. The 130 mutations you mention (which is also wrong -- it should be 65 mutations, the number that occur per copy of the genome, not 130, which is the number per person) counts the number of insertion/deletion events, not the number of base pairs inserted. The Chimpanzee Genome Consortium identified 40 million mutation events, 35 million single base subsitutions and 5 million insertion or deletion events. That number, which includes all of the ~125 Mb you mention, is quite consistent with the observed mutation rate.

Wouldn't you be impressed if a human population was passing on 400 germline mutations per generation. I think I would be checking the area for radiation or some kind of a chemical in the water because it does not normally happen. If it did there would be terrible disease and disorders.

400 germline mutations per generation would be about three times higher than the normal human mutation rate, so yes, I would be surprised. I would not expect terrible disease and disorders unless the elevated mutation rate had been going on a long time, since the rate of new disease-causing mutations is pretty low, so tripling it might be noticable, but would hardly be overwhelming.

But, of course, this mutation rate of 400 per generation doesn't exist. 40 million mutations separating humans and chimpanzees, spread out over ~600,000 generations, requires a mutation rate of 67 germline mutations per generation per genome copy. Which is what it's supposed to be. Yet again, where's the problem?

Ok, humans diverge by .1% and diverge from chimpanzees by at least 4%. Which means that that varitation between humans and chimpanzees is more like 40 times what it is between humans.

Nope. Humans diverge from each other by ~0.1% counting only single-base substitutions. By that measure, humans and chimpanzees differ by 1.2%. If you want to compare the 4% human/chimpanzee difference (which includes indels) to a human-only number, you'll first have to measure the indel polymorphism rate within humans, and there is currently no technology available to do that comprehensively. What we do know is that there is a lot of indel polymorphism out there in humans.

For one thing, if the divergance between humans and chimps was was 1/10 of what it is between humans the divergance between humans and chimps would be 1%. Clearly they are not and I think you are very well aware of that fact. In order to get this level of divergance (3%) would take a fixation of randomly occuring mutations that average of >400 fixed in the population. That is in addition to the fact that they would have had to be cumulative and you act as if I have no evidence that causes a problem for common descent?

I'm afraid all you've got here is evidence of your own confusion. First, as I've just explained above, your numbers do not imply 400 mutations fixing per generation. A divergence of 3% (did you mean 4%?) in total bases implies that 3% x 3 billion base pairs have changed, or 90 Mb. With ~300,000 generations in each lineage, that implies ~150 bp per generation accumulating in each lineage (200 if you meant 4% instead of 3%). That is not the number of mutations per generation, however, since insertion and deletion mutations often change multiple bases in a single mutation, sometimes hundreds of thousands of bases. The number of mutations that separate humans and chimps is 40 million, or about 65 per generation in each lineage.

Second, of course the changes would be cumulative. Aside from that one odd report in a plant, there is no evidence for germ-line changes that aren't cumulative (at least until the mutated base mutates again at some later date).

Do you
1) not understand that I'm saying that mutations must accumulate at a rate of >400 bs per generation?
2) not believe it when we say it?
3) forget it?
4) not care?
5) something else I can't think of?

The answer is (5). What you can't think of is that you're confusing mutation rate with the total number of mutated bases.

The timeframe may not be that long but with populations in the billions the level of divergance should be much higher if they are cumulative.

?? What does the population size have to do with the level of divergence over the last few thousand years? Five thousand years is 250 generations, which should have added about 3000 variant sites to the millions each of us already counts.Why do you expect massive divergence? (Please show your math.)

Before we get to the gene to gene comparisons I wanted to post some quotes and see what, if any response to them you might have.

No. Until we get you past your confusion about mutation rates, I don't see any point to pursuing other questions. They'll just muddy the waters.

 

[rmwilliamsll]

it will function in the same way in the inverted sequence as in the original sequence -- the cell's machinary reads in both directions.

i don't believe this is true. transcription takes place on the antisense DNA strand to make a sense strand of RNA and proceeds 5` to 3`only.
Anti sense RNA appear to be involved as regulatory sequences and transcription factors, not in protein synthesis.

 

[sfs]

it will function in the same way in the inverted sequence as in the original sequence -- the cell's machinary reads in both directions.

i don't believe this is true. transcription takes place on the antisense DNA strand to make a sense strand of RNA and proceeds 5` to 3`only.
Anti sense RNA appear to be involved as regulatory sequences and transcription factors, not in protein synthesis.

No, what I wrote was right, although confusingly worded. Within the inversion, transcription happens exactly as before, with the same sense strand, read from 5' to 3' as before. It's only happening in the opposite direction compared to the rest of chromosome. That is, if before the inversion transcription was from p telomere to q telomere, after the inversion it goes from q to p, and on the opposite strand.

(I hope that's less confusing, but it may not be.)

 

[rmwilliamsll]

No, what I wrote was right, although confusingly worded. Within the inversion, transcription happens exactly as before, with the same sense strand, read from 5' to 3' as before. It's only happening in the opposite direction compared to the rest of chromosome. That is, if before the inversion transcription was from p telomere to q telomere, after the inversion it goes from q to p, and on the opposite strand.

(I hope that's less confusing, but it may not be.)

can you point me towards a reference?
maybe a bit more reading, on my part, will clarify this point.

 

[sfs]

can you point me towards a reference?
maybe a bit more reading, on my part, will clarify this point.

I don't have a reference handy, so let's see if I can do a better job of explaining. Take a chromosome and label one end 'p' and the other 'q'. The chromosome consists of two strands of DNA, which are complementary and which run (chemically speaking) in opposite directions: one strand has its 5' end at p and the other has its 5' end at q. Genes on the chromosome are transcribed from the DNA template ("antisense strand") in the direction 5' to 3', so genes encoded on one strand are read in the direction p to q, and genes on the other strand are read in the direction q to p. Note that either strand can act as the antisense strand -- for some genes one strand acts as the template, and for other genes the other strand does.

An inversion just takes a double-stranded chunk of DNA and turns it around. Suppose a stretch of DNA is like this

3' AAGTTGCTGGGTGTTTTTT 5'
5' TTCAACGACCCACAAAAAA 3'

(where p is to the left and q to the right, and I have bolded the section that will be inverted). After the inversion the DNA will look like this

3' AAGTTGCCACCCATTTTTT 5'
5' TTCAACGGTGGGTAAAAAA 3'

If the bottom strand was being transcribed in the original orientation, the sequence read "ACCCAC" (reading 5' to 3'). After the inversion, the sequence can still be read from 5' to 3' as "ACCCAC", but now by reading the top strand. So the transcribed sequence will be exactly the same within the inversion. Obviously, the transcription start site has to be within the inversion too, or the transcription won't get going in the correct orientation. And of course, if the inversion ends before the gene does, the rest of the transcript will be gibberish.

 

[rmwilliamsll]

Note that either strand can act as the antisense strand -- for some genes one strand acts as the template, and for other genes the other strand does.


thanks
this is what i had wrong.

 

[Ave Maria]

I suggest reading this article from Christian Answers. I do not agree with their entire site but most of their stuff is very good.

http://www.christiananswers.net/q-aig/aig-c018.html

 

[rmwilliamsll]

I suggest reading this article from Christian Answers. I do not agree with their entire site but most of their stuff is very good.

http://www.christiananswers.net/q-aig/aig-c018.html

Similarity ('homology') is not an absolute indication of common ancestry (Evolution) but certainly points to a common designer (creation).

nested hierarchies point to common descent, swapped modules or reuse of tested good functional pieces points to a designer. Chimeras do not exist in nature.

f humans were entirely different from all other living things, or indeed if every living thing was entirely different, would this reveal the Creator to us?

quite to the contrary, if every kind had a different genetic code mapping the triplet DNA codons to tRNA it would be extraordinarily good evidence for a Creator God who created kinds. if human beings had a different code from all other living things or if our genetics was substantially different it would point to a creator not TofE.

If humans were entirely different from all other living things, how would we then live?

depends on the level at which we differ. see my dna->tRNA genetic code example, we would still be able to eat everything else since the basic building blocks are the same.


the rest of the site appears to be similiarily unscientific and a AIG clone.

save time, use talk.origins.

 

[sfs]

I suggest reading this article from Christian Answers. I do not agree with their entire site but most of their stuff is very good.

http://www.christiananswers.net/q-aig/aig-c018.html

At best the article sets the discussion back by six or eight years, since the only data it deals with comes from DNA hybridization experiments. Since then direct comparisons have been made between human and chimpanzee DNA, first by dedicated sequencing of selected regions, and then by means of the full genome sequences of the two species.

Most of the article, however, is an exercise in explaining why we should be ignoring any and all data -- not an approach likely to make scientists happy. It makes no attempt at all to engage any of the real genetic evidence for common descent of humans and chimpanzees.