Humans DNA is 99% similar to that of chimps?

[Assyrian]

Thanks, the figures were back of an envelope, based on some of Mark's numbers, but your selective sweep sounds like what I was thinking about. Cool.

 

[shernren]

Shernren (sp?) has already given the answer to that: random genetic drift. It's a simple concept, really. Suppose I have a new mutation on one of my two copies of a particular gene. I may pass on that one copy to one of my children (meaning the proportion of the population with the mutation would remain unchanged), but I may also pass on zero copies (if I have no children, or if I don't happen to pass on that copy to any of them) or two, three or more copies (depending on how many kids I've got). So the proportion of the population with any variant changes randomly from generation to generation. That's genetic drift.

Because of drift, every site that has two neutral variants will eventually fix one or the other of them. The probability that a particular variant (allele) will fix is just its current frequency. So a 50/50 variant has equal chance of fixing either allele, while a brand new mutation has a very small chance of fixing. Specifically, if there are N individuals in the population, a new mutation has an initial frequency of 1/(2*N), and a probability of fixing of 1/(2*N).

So what is the rate at which new neutral mutations fix? If the probability of a mutation at a given site is u (the mutation rate we've been talking about), then the rate of mutations at that site in the entire population is 2*N*u, that is, every chromosome in the population has an equal shot at mutating each generation. If the rate at which mutations occur is 2*N*u, and the probability that one new mutation will fix is 1/(2*N), the rate at which new mutations fix is 2*N*u / (2*N) = u. Which is why I said the rate at which neutral mutations fix is just the mutation rate.

Spelling's right I get the math, but where does Wiki's "4Ne" estimate come from? Also, am I right to say that specific to the human example, we have on average 32 new mutations showing up per generation, and 32 previously existing neutral mutations being driven to fixation within that same generation, based on the math? Is that the right way to interpret the data? How do I go from there to Wiki's "4Ne" average time taken for a mutation to be driven to fixation?

Also, am I right to say that fixation by selective sweep would occur independently of genetic drift, and thus that the effects of selective sweep would have to be added to the u calculated above to see how fast neutral mutations are actually being fixed?

 

[steen]

I love the study of science and origens, but I dont use it in place of my faith and my belief in the the perfect Word of God.

nobody should. Science says nothing about God.

Most evolutionists are non christian and atheistist

You really need to provide some form of evidence for that claim. As best I know, it is not true.

and we are told by God not to throw pearls before the swine.

An ad hominem? People who accept the biological science are swine or the equivalent? That a rather arrogant, pride-filled claim.

Without Gods presence in iour lives we cannot understand his truths.

And what does this have to do with science?

I place God first and use my study of science to better appreciate the awesome power, intelligence and love He has for me.

Indeed. So why belittle science?

God has revealed himself in nature, through its beauty and design, and God has given me abilities the monkeys will never have including salvation and the promise of eternal life.

Yes, evolution is powerful stuff.

Put your full faith and surrendered life in the hands of God, the only creator and life giver and all truth will be revealed.

Yes? ??? What is the relevance here?

 

[steen]

Other than God being the First cause of the Big Bang,..

Huh? What do you mean? Evolution has absolutely nothing to do with the origin of the universe. Do you understand what Evolution is?

Your argument makes no sense at all. Could you clarify?

 

[steen]

at 20 years generation time that is close to 1.5 nucleotides per year.
and my back of the envelope calculation above was .5 nucleotides per year would account for the information we've read in the articles cited.

And given that a population generally have millions of individuals, the mutations actually carried into the population is small and not at all impossible.

 

[sfs]

I get the math, but where does Wiki's "4Ne" estimate come from?

I don't know of an intuitive explanation for it. If I'm remembering my history correctly, Kimura derived it using a diffusion approximation, and Kingman derived it using a coalescent model. The basic insight is simple: drift happens slower in larger populations, because statistical fluctuations are smaller when you have larger sample sizes. The particular value of 4N (technically 4Ne, but I've been treating the population size as identical to the effective pop size) requires slogging through some more serious math.

Also, am I right to say that specific to the human example, we have on average 32 new mutations showing up per generation, and 32 previously existing neutral mutations being driven to fixation within that same generation, based on the math?

I wouldn't call it "driven", but yes, that's the idea. One catch (a big one in practical terms) is that the fixation rate we've been talking about assumes a constant population size. The human population has expanded enormously of late, and in reality almost nothing is being fixed. Instead, new mutations are accumulating in the population as genetic diversity.

Also, am I right to say that fixation by selective sweep would occur independently of genetic drift, and thus that the effects of selective sweep would have to be added to the u calculated above to see how fast neutral mutations are actually being fixed?

Yes, but only as a temporary fluctuation in the rate. After a sweep, there are no variants left in the population, and nothing fixes for a long time. In the end, it averages out to the same rate (ignoring the particular mutations that are actually selected for -- they fix at a rate faster than the mutation rate).

A useful way of thinking about this sort of thing is to forget about fixation, and to think about comparing a single random human chromosome with a random chimpanzee chromosome. This way you don't have to worry about whether the differences are fixed in the species or are still only partially present in one. (This is in fact how the chimpanzee genome paper analyzed the data.) You can then think of a stretch of DNA as being a single unit handed down from ancestor to ancestor, stretching all the way back to the common ancestor, with some probability of a mutation occurring in it each time it is passed along. For neutral mutations, the number of differences between human and chimp DNA depends only on the number of generations in the two lines and the probability of mutation per generation.

 

[Robert the Pilegrim]

Some of these indels are upwards of 70,000 nucleotides long

And why do you think this is significant?

 

[sfs]

Also, am I right to say that specific to the human example, we have on average 32 new mutations showing up per generation, and 32 previously existing neutral mutations being driven to fixation within that same generation, based on the math?

Clarifying an ambiguity here: if we have on average 32 new mutations per person per generation, we also have on average 32 new fixations for the entire population per generation.

 

[Robert the Pilegrim]

First of all we are not 99% simular to chimpanzees, it is more like 96% simular and about 29% identical in the protein coding genes.

The Chimpanzee Sequencing and Analysis ConsortiumInitial sequence of the chimpanzee genome and comparison with the human genom
Nature 437, 69-87 (1 September 2005)

Orthologous proteins in human and chimpanzee are extremely similar, with approx 29% being identical and the typical orthologue differing by only two amino acids, one per lineage.​

i.e. 29% of functionally identical proteins in chimps and humans are identical and the average difference is 2 amino acids, one from the father and one from the mother.

2 amino acids/protein
DNA Genetic Code Dictates Amino Acid Identity and Order

the protein coded by an average-sized gene (3000 bp) will contain 1000 amino acids​

So the average difference is roughly .2%.

Explain to me why this is shocking and casts doubt on evolution.

 

[shernren]

A useful way of thinking about this sort of thing is to forget about fixation, and to think about comparing a single random human chromosome with a random chimpanzee chromosome. This way you don't have to worry about whether the differences are fixed in the species or are still only partially present in one. (This is in fact how the chimpanzee genome paper analyzed the data.) You can then think of a stretch of DNA as being a single unit handed down from ancestor to ancestor, stretching all the way back to the common ancestor, with some probability of a mutation occurring in it each time it is passed along. For neutral mutations, the number of differences between human and chimp DNA depends only on the number of generations in the two lines and the probability of mutation per generation.

So if I get you right, given that a population is static, the fixation rate is always on average equal to the mutation rate? And thus we can concentrate on how fast mutations are being produced and forget about how fast they are being fixed, given that they are fixed at the same rate they are produced?

Thanks

 

[OObi]

http://www.answersingenesis.org/creation/v19/i1/dna.asp

It's a lot better then myself trying to explain it.

 

[sfs]

http://www.answersingenesis.org/creation/v19/i1/dna.asp

It's a lot better then myself trying to explain it.

That article is outdated: it says that a direct comparison between the chimpanzee and human genomes cannot be made, because the chimp genome hasn't been sequenced yet. It has, now.

More importantly, it doesn't actually address the genetic evidence for common ancestry of humans and chimpanzees. Our overall similarity in DNA is quite weak evidence. The strong evidence comes from the detailed patterns in the differences and similarities. For example, shared pseudogenes, genes that don't actually code for anything because they have been wrecked by a mutation, the same mutation in both chimps and humans. Or the different levels of difference between the species depending on the mutation rate. Mutations that are known to occur frequently make up a large proportion of the differences, while mutations that occur rarely are also rare when comparing the species; this strongly suggests that the differences we see are the result of mutation.

 

[sfs]

That is pretty supprising for me since most of those mutations are neutral while the majority of the rest are deleterious. The thing is that the human race has populations in the billions and the divergence is 1/10 of 1%. With all these generations producing so many mutations it seems a little odd that they are not changing the respective genomes very much at all.

It's only surprising if you don't do any calculations. If a generation produces ~50 new mutations per genome copy, each generation the diversity increases by (2*50)/3,000,000,000, i.e. it goes from 0.1% to 0.100003%. It will take quite a few generations for that to amount to much. (Which of course it has -- that's where the 0.1% comes from, ultimately.)

These are not minor variations in the respective genomes, some of them are as long as 70,000 nucleotides long.

A 70,000 nucleotide insertion that has no effect on fitness is exactly as minor as a 1 nucleotde substitution that has no effect on fitness.

We are not just talking about the random mutations you statistic is based on. These are going to have to be fixed genome wide, how this does not create at least some supprise in the mind of scientists is a mystery to me.

Presumably you mean fixed population-wide, not fixed genome-wide. (The latter doesn't mean anything.) As I have explained to you repeatedly, random neutral mutations do indeed fix in the population, and do so constantly. I have a serious question for you. Why do you keep repeating this argument when it has been knocked down so often? Do you
1) not understand that we're saying that neutral mutations should fix?
2) not believe it when we say it?
3) forget it?
4) not care?
5) something else I can't think of?

So now you turn to indels. Let's see why you think indels should be a problem:

For one thing there are gross structural changes in just over 20% of the protein coding genes in Chromosome 22 alone.

What do you mean, gross structural changes? You cite a result that says that about 20% of proteins differ at all between humans and chimpanzees. The vast majority of these differences are changes to a single amino acid, and usually for a very similar amino acid, or in a part of the protein that has little effect on function. So where are you getting the value of 20% having gross structural changes?

What is the problem? The ones that are neutral are of no concern I suppose, at least at this point. What is most important is that with most mutations that have an effect its deleterious. You have indels happening about 1/5 as frequently as single base substitutions.

Yes, and . . . What? Where's your argument, showing why the observed rate of indels is a problem?

Just out of curiosity what would you expect would be the largerst indel discovered in human genetics? Like I say, I'm just curious and interested to see what you think it might be.

Don't know and don't care. Let's stick to the subject at hand.

I remember the exchange but don't recall agreeing that my argument was wrong. It is still a major problem for TOE in my mind and I have yet to see a demonstrated or directly observed mechanism for fixing the indels on this level.

Neutral genetic drift is an observed (and inevitable) mechanism for fixing indels at whatever rate they occur at. So where's the problem?

I really would like to move on from the gross number of mutations throughout the respective genomes.

No. You made an argument (and have made it many times, despite correction). Back it up. Explain why the rate of indels is a problem, or stop using the argument -- and not just when you're challenged.

At any rate, it is exciting to see you again Professor. It's the opportunity to have these discussions with world class scientists like yourself that keeps me fascinated with this subject.

I'm not a professor; I'm a staff scientist. Mostly I'm just Steve, though.

 

[mark kennedy]

It's only surprising if you don't do any calculations. If a generation produces ~50 new mutations per genome copy, each generation the diversity increases by (2*50)/3,000,000,000, i.e. it goes from 0.1% to 0.100003%. It will take quite a few generations for that to amount to much. (Which of course it has -- that's where the 0.1% comes from, ultimately.)

It's kind of difficult to get the concept down pat since we are looking at some pretty random alterations. I was under the impression that the effect on fittness was the prize in evolutionary change, particularly adaptive evolution. So you have 50 new mutations per generation as they appear at random with most of them doing absolutly nothing. With the population size of humans numbering in the billions and since they inhabit every ecological niche on the planet it seems like these mutations would be accumulating. They are supposed to have in our previous lineage and yet our genomes are fairly uniform.

Not a lot there to calculate from my perspective, perhaps I'm missing something here.

A 70,000 nucleotide insertion that has no effect on fitness is exactly as minor as a 1 nucleotde substitution that has no effect on fitness.

I was under the impression that mutations happened at random and had just as much chance of occuring in functional/protein coding regions as, say, a gene desert. There are indels in the coding areas including gross structural changes (actually just differences).

Presumably you mean fixed population-wide, not fixed genome-wide. (The latter doesn't mean anything.) As I have explained to you repeatedly, random neutral mutations do indeed fix in the population, and do so constantly. I have a serious question for you. Why do you keep repeating this argument when it has been knocked down so often?

Actually all I have heard in response is that the differences in the genomes accumulated because they can and must have. That is about it. I am often contradicted but I have yet to see anything remotely resembling a demonstrated mechanism for producing alterations in the nucleotide sequence genome/population wide or whatever you want to call it.

Do you
1) not understand that we're saying that neutral mutations should fix?

I can understand that they are not going to be wiped out in a selective sweep if that's what you mean. I am still wondering if these neutral mutations are accumulating so rapidly then why aren't human genetics changing on a massive scale?

2) not believe it when we say it?

I don't believe neutral and slightly deleterious mutations account for the differences between chimps and humans.

3) forget it?

No, it is firmly impressed upon my mind, it's just not an explanation.

4) not care?

I don't care that much about neutral effects from mutations. I am very interested in positive selection and adaptations that result from changes in the protein coding, regulatory, outlier...genes. Neutral is just that, it is neutral and I am not impressed with the fact that they tend to accumulate.

5) something else I can't think of?

I'm not really sure if I am saying this right but there are going to have to be adaptive traits accumulated as a result. I'm still waiting to learn how that actually works.

So now you turn to indels. Let's see why you think indels should be a problem:


What do you mean, gross structural changes? You cite a result that says that about 20% of proteins differ at all between humans and chimpanzees. The vast majority of these differences are changes to a single amino acid, and usually for a very similar amino acid, or in a part of the protein that has little effect on function. So where are you getting the value of 20% having gross structural changes?

The chromosome 22 comparison paper was were the original statistic came from:

"83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level.

A total of 140 of these 179 genes show amino acid replacements, but no gross structural changes are expected...

...In contrast, 47 PTR22q genes show significant structural changes affecting at least one of their transcript isoforms. Fifteen genes have indels within their coding region yet retain frame consistency in all but one case (TCP10L)..

Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins"

http://www.nature.com/cgi-taf/DynaP...full/nature02564_r.html&filetype=&dynoptions=

Yes, and . . . What? Where's your argument, showing why the observed rate of indels is a problem?

You seem to have reconciled the mutation rate to the SNPs but don't seem to have an explanation for the indels. Indels cause devastating diseases, not adaptive traits but they were accumulated by the dozens every generation for millions of years. It doesn't make any sense that we have a common ancestor with chimps if the genetic divergance is too great.

Don't know and don't care. Let's stick to the subject at hand.

If you say so.

Neutral genetic drift is an observed (and inevitable) mechanism for fixing indels at whatever rate they occur at. So where's the problem?

Because this is not drift, its radical divergance.

No. You made an argument (and have made it many times, despite correction). Back it up. Explain why the rate of indels is a problem, or stop using the argument -- and not just when you're challenged.

90 million divided by 5 million, do the math.

I'm not a professor; I'm a staff scientist. Mostly I'm just Steve, though.

Ok, out of time again...sorry

 

[steen]

It's kind of difficult to get the concept down pat since we are looking at some pretty random alterations. I was under the impression that the effect on fittness was the prize in evolutionary change, particularly adaptive evolution. So you have 50 new mutations per generation as they appear at random with most of them doing absolutly nothing.

It probably is more than that, but lets use it for examples sake.

With the population size of humans numbering in the billions and since they inhabit every ecological niche on the planet it seems like these mutations would be accumulating.

Not without Natural Selection to push for their increase. Their presence otherwise would be fairly constant. In some individuals they would appear, in others not, and on average they wouldn't really change much at all in how much they are concentrated in the population. There might be a bunch of them, but normally only in small amounts.

Now, if one of them, f.ex. would result in remarkable adaptation to the cold, and we end up with a nuclear or meteoric "winter," then suddenly this would change and this very minorly represented gene suddenly would start being increased significantly in the population.

Other mutations were helpful, but per medicine has been rendered somewhat irrelevant, such as the Sickle-cell genetic change(s). They resulted in carrier status resistance to malaria, and in populations of humans in malaria-infested areas, they have increased to about 10% of the population. Immigrants to the US, however, really have no benefit from the gene, and the percentage in the population has not been increasing like it has in areas where malaria is still a problem as is medical supplies.

And then, mutations that are neutral, but are sitting next to other mutated segments of the DNA or chromosome are sometimes carried along for the ride, so to speak.

They are supposed to have in our previous lineage and yet our genomes are fairly uniform.

Not that similar. But those that were beneficial have more or less spread throughout the population, while the neutral ones only sit around in small local, generally unchanged populations.

I was under the impression that mutations happened at random and had just as much chance of occuring in functional/protein coding regions as, say, a gene desert. There are indels in the coding areas including gross structural changes (actually just differences).

There are parts of the genome that is very stable and really haven't seen any changes. Remember that we share something like 70% of the genes with starfish. Those 70% really never change.

Actually all I have heard in response is that the differences in the genomes accumulated because they can and must have. That is about it.

We have followed these genetic changes as they have accumulated, even in modern time, since Darwin. Rest assured that if you actually looked at the scientific literature, you will find these documented.

And no, science does not publish just to prove creationists wrong. that is the lest of their concerns. they publish because they find evidence or because the medical exploration confirms the data. Sickle-cell research or research into gaucher's disease, f.ex., are for medical purposes. The research is accepted because it is documented, confirmed, and shows its value in accuracy in real life. No creationist claim can contradict that.

I am often contradicted but I have yet to see anything remotely resembling a demonstrated mechanism for producing alterations in the nucleotide sequence genome/population wide or whatever you want to call it.

That would be mutations and natural selection of that gene or its neighbor.

I can understand that they are not going to be wiped out in a selective sweep if that's what you mean. I am still wondering if these neutral mutations are accumulating so rapidly then why aren't human genetics changing on a massive scale?

Well, it is but only to some extend. We see lots of changes in the human genotype, but not many that matter in the human phenotype.

I don't believe neutral and slightly deleterious mutations account for the differences between chimps and humans.

But positive mutations over the last 3-10 million years certainly could. Remember that BOTH populations changed. It is not just hominids that mutated and changed.

I don't care that much about neutral effects from mutations. I am very interested in positive selection and adaptations that result from changes in the protein coding, regulatory, outlier...genes.

So you are talking about Natural Selection.

I'm not really sure if I am saying this right but there are going to have to be adaptive traits accumulated as a result. I'm still waiting to learn how that actually works.

Sickle-cell mutations is a good example. Here is the PBS short version:
http://www.pbs.org/wgbh/evolution/library/01/2/l_012_02.html

Here is an explanation from a medical site. Go to section III, Genetic Variability in Host Response to Malaria quite a bit down the page 50%+):
http://www.asheducationbook.org/cgi/content/full/2002/1/35

At the end of it is this:
...Evolutionary Implications
As we have seen, a recurrent pattern is emerging for the distribution and molecular pathology of the human malaria-related polymorphisms. Despite the remarkable degree of protection offered against heterozygotes by the sickle cell gene, and its frequent appearance in Africa, the Middle East, and India, it has never been found farther east than India. Similarly, although Hb E reaches extremely high frequencies throughout Southeast Asia, it is not seen farther west than the eastern parts of the Indian subcontinent. Recent studies of the ß globin gene haplotypes associated with the ßS Senegal mutation have suggested that it is recent (45-70 generations) in origin.49 Both the

and ß thalassemias occur throughout the tropical climes, with the exception of Central and South America, but in each of the high-frequency populations there are different sets of mutations; their relationships to haplotypes of the ß globin gene suggest that the expansion of the ß thalassemia mutations must have occurred fairly recently. Indeed, all these observations are in keeping with the notion that whatever has been responsible for achieving the extraordinarily high gene frequencies for these conditions has been of fairly recent origin.
Recent studies of haplotype diversity and linkage disequilibrium at the human G6PD locus provide further evidence of the recent origin of alleles that confer malarial resistance.50 In an analysis of 2 G6PD haplotypes, it was found that 2 common variants appeared to have evolved independently between 3000 and 11,000 years ago. These observations on the fairly recent, in evolutionary terms, appearance of genetic polymorphisms that confer resistance to malaria are in keeping with estimates of the spread of P. falciparum derived from studies of polymorphic systems of the parasite. For example, a recent analysis of 25 intron sequences of P. falciparum, involving both general metabolic and housekeeping genes, showed very few nucleotide polymorphisms and suggested that the parasite originated in something like its present form between 9000 and 20,000 years ago.51 These figures are in general agreement with other studies of polymorphic genes of P. falciparum.52 This timescale is in keeping with the notion that it was the development of agriculture somewhere between 5000 and 10,000 years ago that provided the conditions necessary for the effective spread of malaria. ...

Then there is this one talking about the spread of the gene and its local variations, tying it to disease pressure etc:
http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijhe/vol1n2/sickle.xml

And there are lots more. As you can see, this is a direct tie-in between evolution and medicine. medicine bases its research and findings specifically on evolution in this case.

 

[shernren]

It's kind of difficult to get the concept down pat since we are looking at some pretty random alterations. I was under the impression that the effect on fittness was the prize in evolutionary change, particularly adaptive evolution. So you have 50 new mutations per generation as they appear at random with most of them doing absolutly nothing. With the population size of humans numbering in the billions and since they inhabit every ecological niche on the planet it seems like these mutations would be accumulating. They are supposed to have in our previous lineage and yet our genomes are fairly uniform.

Not a lot there to calculate from my perspective, perhaps I'm missing something here.

...

I can understand that they are not going to be wiped out in a selective sweep if that's what you mean. I am still wondering if these neutral mutations are accumulating so rapidly then why aren't human genetics changing on a massive scale?

Selective sweeps fix neutral mutations, not wipe them out. We're talking about genetic drift which is a completely different mechanism from natural selection. Imagine this: Let's say Adam had a hemoglobin-A allele and a hemoglobin-B allele. And let's say that he had just 4 sons. Can I say with any certainty that 2 have the A allele and 2 have the B allele? No - for all we know, 3 got A and 1 got B. In one generation the A:B allelic ratio goes from 50:50 to 75:25, and if the son who has B gets struck by lightning or mauled by a lion or something, then instantly the A allele would have been fixed.

Why does a random event have such large ramifications? Because the smaller a set of genomes, the larger effect random occurrences have on their allelic distributions. If I have just 3 boys with A alleles and 1 boy with a B allele it's easy to imagine something which would have killed the solitary boy. If I have 3 billion humans with A alleles and 1 billion humans with B alleles, however, it's hard to imagine a catastrophe which would wipe out the B-allele carriers in one shot without wiping out the rest of humanity - especially since there is little to no advantage difference between A and B.

The chromosome 22 comparison paper was were the original statistic came from:

"83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level.

A total of 140 of these 179 genes show amino acid replacements, but no gross structural changes are expected...

...In contrast, 47 PTR22q genes show significant structural changes affecting at least one of their transcript isoforms. Fifteen genes have indels within their coding region yet retain frame consistency in all but one case (TCP10L)..

Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins"

http://www.nature.com/cgi-taf/DynaPa...e=&dynoptions=

You've been talking about human genomics and arguing from that aspect for longer than I've even been on the board. And yet you haven't checked the source?

http://www.nature.com/nature/journal/v429/n6990/extref/nature02564-s2.doc

Refer to Supplementary Tables 4 and 5, I'll walk you through them. The important column is "genomic changes in PTR22q", which says how the chimp genome differs from ours. The first column "human gene references" states which human gene it was compared to, and the third column "AA [amino acid] indels in chimp" state the amino-acid changes to the protein involved. I'm not sure what to do with the mouse ortholog in the context of our discussion.

Here goes. There are fifteen proteins in this table. First impression: that's very few proteins to raise hue and cry about.

Out of those fifteen, four show an insertion of three base pairs, or one codon, which is equivalent to the insertion of one amino acid into the protein sequence. One has an insertion of two codons, one has an insertion of three, one has an insertion of four, and one has an insertion of five. Three have a deletion of one codon, one has a deletion of two, one has a deletion of three with an insertion of three, and one has a deletion of 65 codons. (That one is pretty big, I'll grant.)

Besides the massive 65-codon deletion, the total change comes up to a difference in 29 codons, for a total of 94 codons' change. For comparison, insulin, which was the first protein to have its primary structure elucidated, has about 51 amino acids in final form - and that's after posttranslational modification, in which another 60-70 odd (OTOH) amino acids coded for in the genome are cut off. In this context, 94 codons amounts to a complete change in one protein. Just one.

On to Supplementary Table 5. It lists 32 proteins. 25 of these have a single-nucleotide substitution, insertion, or deletion. 2 have 2-base insertions. There is one deletion of 10 bases, one of 16 bases, one of 38 bases, one of 40 bases, and one of 1287 bases. (Again, the 1287 bases is a huge mutation.) Besides the 1287 bases modification, there are another about 140 bases' worth of modification, making for about 1420 bases' worth of modification. The reason I'm rounding is because 33.3 megabases were compared. How significant is 1420 bases different out of 33 million bases tested? (If you're wondering why they're called "gross structural changes" when they're so small in genomic terms, go find out yourself! Hint: divide each of these numbers - 1, 2, 10, 16, 38, 40 - by 3.)

Also, check this out: http://www.nature.com/nature/journal/v429/n6990/extref/nature02564-s4.htm ... while I do want to look at the original research, looking through all those divergences is really too tedious for me, especially since I've treated the most important ones already. If you find anything doubtful in this data, let me know. The easiest thing to do would be to obtain the mean and standard deviation of the divergence of the chimp genes from the human ones. My extremely rough estimate is that the mean is going to be around 3% difference with a standard deviation of probably 2%. Significantly higher than the good old 98.5% estimate, but no ironclad creationist proof.

Every time you provide a source, it seems to say exactly the opposite of what you wanted to prove. Now I'm waiting to see what evidence you have that indels happened too fast in human evolution. Do you have any research that measures how fast indels happen in current observation?

 

[Robert the Pilegrim]

I think the obvious should be stated here, biologists do not fully understand how evolution occurs.

That said, the gluing together of chimp chromosomes 2 and 3, the common broken vitamin C genes, various other evidence, is very strongly in favor of common descent for humans and chimps...

The chromosome 22 comparison paper was were the original statistic came from:

"83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level.

A total of 140 of these 179 genes show amino acid replacements, but no gross structural changes are expected...

...In contrast, 47 PTR22q genes show significant structural changes affecting at least one of their transcript isoforms. Fifteen genes have indels within their coding region yet retain frame consistency in all but one case (TCP10L)..

Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins"

http://www.nature.com/cgi-taf/DynaP...full/nature02564_r.html&filetype=&dynoptions=

FWIW, if I am reading figure 2 correctly, of the 68,000 indels less than 2000 are longer than 20 bp.

Sfs, what light do you think figure 3 sheds on this?

 

[mark kennedy]

It probably is more than that, but lets use it for examples sake.

Not without Natural Selection to push for their increase. Their presence otherwise would be fairly constant. In some individuals they would appear, in others not, and on average they wouldn't really change much at all in how much they are concentrated in the population. There might be a bunch of them, but normally only in small amounts.

Ok, that would be the generalities and I have long understood the speculation about what if. Natural selection is actually the death of the less fit, nothing more. Elaborate scenerios are created for the primordial past using the rethoric of Darwinism but lets see where you are going with this.

Now, if one of them, f.ex. would result in remarkable adaptation to the cold, and we end up with a nuclear or meteoric "winter," then suddenly this would change and this very minorly represented gene suddenly would start being increased significantly in the population.

You are assuming that this kind of an adaptation requires some kind of a change in the genes. I'm not sure that this is a requirement for adapting to a cold climate. What is more you are assuming a meteoric winter that is again speculative. Nevertheless, lets see where you are taking me with this.

Other mutations were helpful, but per medicine has been rendered somewhat irrelevant, such as the Sickle-cell genetic change(s). They resulted in carrier status resistance to malaria, and in populations of humans in malaria-infested areas, they have increased to about 10% of the population. Immigrants to the US, however, really have no benefit from the gene, and the percentage in the population has not been increasing like it has in areas where malaria is still a problem as is medical supplies.

Sickle-cell is a genetic mutation that results in a deformed blood cell, it's not an adaptation. It does help to slow the spread of the infection but I see no reason to consider this an adaptation. An improvement in the immune system on the other hand sometimes includes altered genetic codes but I don't have a lot of the details about this.

And then, mutations that are neutral, but are sitting next to other mutated segments of the DNA or chromosome are sometimes carried along for the ride, so to speak.

While I understand the simple truth in your statement I'm not entirely sure what you are getting at. Sure, neutral mutations in noncoding/nonfunctioning parts of the genome are less likely to be subject to a selective sweep if that's what you mean.

Not that similar. But those that were beneficial have more or less spread throughout the population, while the neutral ones only sit around in small local, generally unchanged populations.

The beneficial ones could if they were germline mutations rather then somatic. In some experiements they found that what is a neutral or deleterious mutation when resources are plentifull, can be beneficial when resources are scarce. However, when the surviving population is reintroduced to plentifull resources the minority with the benefical effect from a mutation lose their advantage.

There are parts of the genome that is very stable and really haven't seen any changes. Remember that we share something like 70% of the genes with starfish. Those 70% really never change.

I know what you mean here, I think that is refered to as transposable vs. conserved regions. It will be nice when science moves far enough ahead to give us a clearer picture of what particular genes do and how much they can withstand change.

We have followed these genetic changes as they have accumulated, even in modern time, since Darwin. Rest assured that if you actually looked at the scientific literature, you will find these documented.

First of all when Darwin wrote On the Origin of Species he noted phenotypic traits only. The chromosome would not be directly observed untill the turn of the century almost 50 years later. There are documented instances where altered pheotypes have a selective advantage but this tends to be cyclical rather then cumulative.

And no, science does not publish just to prove creationists wrong. that is the lest of their concerns. they publish because they find evidence or because the medical exploration confirms the data. Sickle-cell research or research into gaucher's disease, f.ex., are for medical purposes. The research is accepted because it is documented, confirmed, and shows its value in accuracy in real life. No creationist claim can contradict that.

I never said that creationists are specially targeted by natural science. It is natural history that specifically rejected God as an explanation for any point of origin in the natural world. Science itself is being defined as excluding God at any level which is neither scientific nor natural. Science is about demonstrated and directly observed processes and theology at one time was the queen of the sciences. Now there are those who assume science and theology are in conflict and it's not creationists that are creating this illusion.

That would be mutations and natural selection of that gene or its neighbor.

In order for an altered gene to be 'selected' it has to first be produced and then provide an advantage. The result would be that the 'less fit' simply die off thus establishing the new trait in the surviving population.

Well, it is but only to some extend. We see lots of changes in the human genotype, but not many that matter in the human phenotype.

Actually, I would have said that the other way. The phenotype can change without the genotype changing at all. Certain genes can be turned on and off, certain ones involved in size, shape, color, texture...etc can change their frequency of expression. This is the thing though, genetically mutations tend to be neutral or deleterious particularly when they affect vital organs like the brain and liver.

But positive mutations over the last 3-10 million years certainly could. Remember that BOTH populations changed. It is not just hominids that mutated and changed.

For human evolution we are talking 5-7 million years and I could stretch this out to ten million years. In say, 5 million years you accumulate 5 million indels adding up to 90 million nucleotides. Your speculative scenerio of the establishing of mutations (neutral, deleterious, beneficial) does not account for populations accumulating mutations on this level. That comes to 1 indel per year for ten million years, you do the math.

So you are talking about Natural Selection.

Sickle-cell mutations is a good example. Here is the PBS short version:
http://www.pbs.org/wgbh/evolution/library/01/2/l_012_02.html

Yes, I have seen Sickle-cell used as an example of a beneficial mutation more times then I can count. You seem oblivious to the fact that this is resulting in a deformed blood cell, not improved immune systems. There is another example that is supposed to provide an imporved resistance to HIV. When looking at the literature on it I found that this particular mutation was resulting in a defective receptor that does not allow the HIV virus to latch onto the T-cell. My point is a deformed blood cell and a defective receptor is not an adaptive trait. Improved fittness is the prize in the natural world and mutations rarely provide such a thing and almost never without sever consequences.

Here is an explanation from a medical site. Go to section III, Genetic Variability in Host Response to Malaria quite a bit down the page 50%+):
http://www.asheducationbook.org/cgi/content/full/2002/1/35

I don't have time to search the resource material right now, I'll have to rely on your commentary.

Then there is this one talking about the spread of the gene and its local variations, tying it to disease pressure etc:
http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijhe/vol1n2/sickle.xml

And there are lots more. As you can see, this is a direct tie-in between evolution and medicine. medicine bases its research and findings specifically on evolution in this case.

I have seen more of this then I care to remember. I am far from convinced that a deformed blood cell is a beneficial effect from a mutation. How many living systems with blood cells running through their veins have evolved anything other then round blood cells?

Sure there is a slight advantage, that is when the population is exposed to malaria. However, this is not an adaptation nor is it positive selection as I understand it.

 

[rmwilliamsll]

HbS is not the only mutation of Hb that confers some resistance to malaria. There are 100's of them and if you map the mutations to a map of endemic malaria they are the same. NS is selecting for malaria resistance, despite the problems associated with being homozygous for most of these mutations.

I never said that creationists are specially targeted by natural science. It is natural history that specifically rejected God as an explanation for any point of origin in the natural world. Science itself is being defined as excluding God at any level which is neither scientific nor natural. Science is about demonstrated and directly observed processes and theology at one time was the queen of the sciences. Now there are those who assume science and theology are in conflict and it's not creationists that are creating this illusion.

The problem is that we can not see God. We can not touch Him, nor in any other physical way show any interaction with Him. The knowledge of God is basically private and inaccessible to people who have not had those experiences, making it very subjective. It is fundamentally incommenserate with scientific procedure which is very public and intersubjective.

Since A.Kuyper there has been a consistent cry for a Christian science, how do you build such a thing? If access to God is via experiential, private and subjective means?

 

[steen]

Ok, that would be the generalities and I have long understood the speculation about what if. Natural selection is actually the death of the less fit, nothing more.

Not exactly. It is that a more "fit" gene will end up increasing its prominence in a population in each generation subsequent to its mutational origin.

It is not that the less fit die; it is that they don't have, relatively, as many offspring making it to their own reproduction.

Elaborate scenerios are created for the primordial past using the rethoric of Darwinism but lets see where you are going with this.

I am not sure I can agree with your claim. "Primordial" usually is a reference to Abiogenesis or other "origin of life" speculations. This is not part of Evolution, nor of Darwin's original hypothesis, so I don't feel you can pair this concept with "Darwinism."

You are assuming that this kind of an adaptation requires some kind of a change in the genes.

Not at all. As the Peppered Moth research showed, it can also be a change in the distribution of an already existing gene (or several). It requires a change in the gene expression of the population, if that is what you meant.

I'm not sure that this is a requirement for adapting to a cold climate.

genetic changes are involved in a population adapting to colder climates. hair growth, fat distribution, body build, VitC absorption etc.

What is more you are assuming a meteoric winter that is again speculative. Nevertheless, lets see where you are taking me with this.

Well, more as an illustrative example of something that could cause a cold period that could result in a change in the environment and thus a reason fr a change in the genetic expression in a population.

Sickle-cell is a genetic mutation that results in a deformed blood cell, it's not an adaptation. It does help to slow the spread of the infection but I see no reason to consider this an adaptation.

If it keeps people from getting malaria, and thus makes it easier for them to live long enough to have offspring, then it certainly is an adaptation over getting malaria an dying young.

An improvement in the immune system on the other hand sometimes includes altered genetic codes but I don't have a lot of the details about this.

The result would be the same. Actually, the immune system is a very good analogy to how evolution works. If a change in the environment (an allergen) is introduced, the genetic expressions change and some of the multiple genetic changes (in this case, the flurry of antibodies released) will function better than others and end up dominating.

While I understand the simple truth in your statement I'm not entirely sure what you are getting at. Sure, neutral mutations in noncoding/nonfunctioning parts of the genome are less likely to be subject to a selective sweep if that's what you mean.

Yes, that was my point.

The beneficial ones could if they were germline mutations rather then somatic. In some experiements they found that what is a neutral or deleterious mutation when resources are plentifull, can be beneficial when resources are scarce. However, when the surviving population is reintroduced to plentifull resources the minority with the benefical effect from a mutation lose their advantage.

That would be true, and then the prominence of that genetic mutation/variation will loose prominence again in that population.

I know what you mean here, I think that is refered to as transposable vs. conserved regions. It will be nice when science moves far enough ahead to give us a clearer picture of what particular genes do and how much they can withstand change.

Correct and agreed.

First of all when Darwin wrote On the Origin of Species he noted phenotypic traits only. The chromosome would not be directly observed untill the turn of the century almost 50 years later.

Correct. but we certainly can trace mutations backward in time. A fascinating example is the gaucher Disease, a disease of lack of enzymes that break down fat in cells (It is related to Tay-Sacks). It comes in 3 different subtypes, one of which is mainly found in Sweden and can be tracked back directly to mutations in one single family back in the 1500's.

There are documented instances where altered pheotypes have a selective advantage but this tends to be cyclical rather then cumulative.

Sure. originally, the focus was mainly on the Natural Selection part. It was known that there was something else there, but it wasn't specifically known until DNA and genes were discovered.

I never said that creationists are specially targeted by natural science.

Sorry, I misunderstood you , then. My apologies.

It is natural history that specifically rejected God as an explanation for any point of origin in the natural world.

Rather, Natural Science accept only what can be shown through evidence Science doesn't reject God as an explanation. Rather, it says that it can't find any actual evidence of God's involvement. Science is not all-encompassing enough to explore a concept like God, and as such is unable to provide evidence either way. Science deals only in the evidence.

Science itself is being defined as excluding God at any level which is neither scientific nor natural.

I must disagree with your characterization of science. reputable scientists or scientific agencies/institutions/journals would never make such a claim, as there would be no evidence to support it.

Rather, science is defined as the exploration of the physical world (or of things that can be observed or measured) through the application of the Scientific Method.

Science is about demonstrated and directly observed processes and theology at one time was the queen of the sciences. Now there are those who assume science and theology are in conflict and it's not creationists that are creating this illusion.

Well, yes it is actually. Science merely states that it can't say anything about God one way or the other, that there is no evidence for the existence of God. Creationists come in and claim that science is wrong because it doesn't 100% confirm Genesis 1. It is not science which levels accusations, other than post-hoc to creationist false claims.

In order for an altered gene to be 'selected' it has to first be produced and then provide an advantage. The result would be that the 'less fit' simply die off thus establishing the new trait in the surviving population.

Other than it doesn't have to result in a die-off, this is essentially correct. It might help you if you think of Evolution as prominence of genes in a population rather than as the fate of individual organisms.

That is why the axiom is that populations evolve, individuals don't.

Actually, I would have said that the other way. The phenotype can change without the genotype changing at all. Certain genes can be turned on and off, certain ones involved in size, shape, color, texture...etc can change their frequency of expression.

My point is that we see lots of neutral mutations that have no effect on the phenotype, while each of these changes does represent a change in the genotype.

This is the thing though, genetically mutations tend to be neutral or deleterious particularly when they affect vital organs like the brain and liver.

certainly. that is what keeps populations more or less uniform. If most mutations lead to big changes, we really would end up with a lot more different species (ultimately to the point of every individual as an individual species as well).

It is like gas in a solid container. Lots of movement, lots of pressure to change in all directions, but as long as the environment is stable, so is the population, the gas as a whole. Now, make a hole in the side of the container (ie. a change in the environment, a new niche). You will then see a large amount of change until a new equilibrium is reached

For human evolution we are talking 5-7 million years and I could stretch this out to ten million years. In say, 5 million years you accumulate 5 million indels adding up to 90 million nucleotides. Your speculative scenerio of the establishing of mutations (neutral, deleterious, beneficial) does not account for populations accumulating mutations on this level. That comes to 1 indel per year for ten million years, you do the math.

remember that you loose some as well, and that (esp. today with international mobility), the changes tend to spread rapidly and become part of a more uniform population than on the past.

The contrary example is that of ring-species of which we have several documented examples. I don't know if you are familiar with these? (A species spread out along a barrier such as a mountain or the north pole or such)and change slightly but still is inter-breadable with the original species. Next, these move further etc, with slight changes every time, until the circle is completed and the populations meets specimens of the original population and no longer is breeding-compatible. We have two species at the intersect. Essentially, all the populations between these two groups are the "transitional" forms that don't quite provide a complete intermingling of genes..

Yes, I have seen Sickle-cell used as an example of a beneficial mutation more times then I can count. You seem oblivious to the fact that this is resulting in a deformed blood cell, not improved immune systems.

It doesn't have to result in improved immune systems. It has to result in improved survival. If the carriers have improved survival because the infected cells rupture and kill the parasite, then they are more likely to end up having offspring than are those who get infected and do not have the trait, because these people remain infected and die instead. Thus, the mutation of the sickle-cell makes it more likely for the carrier to have successful reproduction, and that gene then increases proportionally in the population. It is about Natural Selection, not "improved immune system."

There is another example that is supposed to provide an imporved resistance to HIV. When looking at the literature on it I found that this particular mutation was resulting in a defective receptor that does not allow the HIV virus to latch onto the T-cell. My point is a deformed blood cell and a defective receptor is not an adaptive trait.

If it prevents infection, and thus makes it more likely for the person to live longer and have more offspring, then yes it very much is. remember, we are not talking about the "health" of an individual. We are talking about their ability to have offspring and pass the gene on to the next generation. When proportionally more with a mutation survives to have offspring, then that is a "positive" mutation.

Improved fittness is the prize in the natural world and mutations rarely provide such a thing and almost never without sever consequences.

i think you have gotten hung up on the term "fitness." It is about improved fitness TO HAVE OFFSPRING. If you have relatively more offspring because of the mutation (such as living longer or into reproductive age), then it gives you a "competitive advantage" and thus is a "more fit" mutation.

I have seen more of this then I care to remember. I am far from convinced that a deformed blood cell is a beneficial effect from a mutation. How many living systems with blood cells running through their veins have evolved anything other then round blood cells?

They evolved blood cells that rupture if infected with the malaria parasite, thus preventing it from reproducing in your body. Thus the carrier has a better chance of survival and therefore an relative improved chance of having babies. Competitive advantage over those without the mutation in any area with malaria.

Sure there is a slight advantage, that is when the population is exposed to malaria.

Which is the very point. If you have the mutation there, you are less likely to die from malaria, and thus more likely to have kids.

However, this is not an adaptation

Sure it is. A genetic change that results in improved survival and thus improved chance of reproduction.

nor is it positive selection as I understand it.

I hope my post have clarified it so you can see how it is. This is exactly what Evolution is all about. A response to the environment, resulting in enhanced chances for having offspring.