Gene Number Changes Between Humans and Chimps

mark kennedy said:

First of all Wikipedia is a source like Creationist websites or Talk Origins, good starting point but hardly primary source documentation. You have no idea what I have read or what I know because all you need to know about me is that I'm a YEC and you are immediately considering yourself my intellectual superior. Naraoia has not adequately responding but then again he is not required to do so unless it interests him.

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Her, if that's me

Not adequately responded to what? That you completely confused substitutions and frame shifts?

BTW, I think TalkOrigins is a very good source, much better than Wikipedia in many cases, if only because it has wonking huge reference lists.

Again, you would not have the slightest idea what I understand and what I don't. This is typical of the two a priori assumptions of Darwinian metaphysics. First, the a priori assumption of universal common ancestry by exclusively naturalistic causes (naturalistic assumptions). If you refuse to make the first assumption then the second one is that you are arguing from incredulity (ignorance).

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Sorry, what? If memory serves, Mystman commented on your mangling of well-known biological concepts. Confusing basic concepts of molecular genetics has nothing to do with common descent or arguments from incredulity (everything to do with ignorance, however).

And sorry, universal common descent by "naturalistic causes" is a conclusion, not an assumption, and hardly metaphysics as I understand the word.

I have studied the scientific literature regarding human evolution both in genetics and paleontology. Unlike the typical poster on here I don't rely on Talk Origins, Creationist websites, Wikipedia and pedantic satire for the substance of my arguments.

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Which would be a great thing, provided that you understand the scientific literature, but to be honest, I'm becoming less and less sure of that.

This individual will be limited to the point made previously by the evolutionists who make the initial contact which is Naraoia's primary difficulty except he is probably not aware of it.

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I'm sorry, what (again)? If you want to know, I hate repeating what others said unless I think it's worth repeating/adding to. Unfortunately, sometimes there's only one way you can say someone's wrong.

And I don't see how repeating a good point is bad, either. I suggest you consider the content of our posts rather than tallying repetitions.

Naraoia seems genuinely curious but has picked up on a fallacious thesis that 'chimpanzees and humans are 98% the same in their DNA'.

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I have not, and if I have, please show me where I said so. I don't really care precisely how similar we are. Which is why I honestly have no idea what the most recent estimates are for orthologous sequences or for whatever else anyone cares to measure similarity on. So, my bad if I default to what I've heard most often, but I don't think I've positively stated that 98% is Teh Right Number.

What I do care about is that your basis of declaring the 98% estimate wrong in this thread was fallacious. You can say 98% is wrong, but not by quoting an estimate that measures a completely different thing and thus can't possibly refute it.

When the paper discussed in the OP says that the 98% still holds true depending on the comparison you have to understand what they mean by that:

To understand the genetic basis of the unique features of humans, a number of pilot studies comparing the human and chimpanzee genomes have been conducted. Estimates of nucleotide substitution rates of aligned sequences range from 1.23% by bacterial artificial chromosome (BAC) end sequencing3 to about 2% by molecular analysis, whereas the overall sequence difference was estimated to be approximately 5% by taking regions of insertions or deletions (indels) into account. (Nature 429, 382-388 27 May 2004)
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See? I bolded the bit that says what the 98% measures. And their own estimate (1.44%) for the same thing is within that range. (Now every time you link to a paper, I'm going to check it. I no longer trust your ability to correctly present what they say)

Do note that this comparison indicated that 20% of the protein coding sequences show gross structural changes, which is nothing more then major structural differences.

Taken together, gross structural changes affecting gene products are far more common than previously estimated (20.3% of the PTR22 proteins, as listed in Supplementary Tables 4 and 5). In addition, 87 genes in the catalogue show mutations in at least one of the splice sites. (Nature 2004)
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Gross structural changes based on a small number of mutations.

What was the minimum sequence identity they found? 83%, and a substantial subset of those genes - 179 out of 231 - was over 99% identical at the nucleotide level.

Don't start mixing the amount of change with the amount of mutations. Again, they are different things, and if your argument is that we are too different amount-of-mutation-wise, then the nature of the changes effected by those mutations is irrelevant.

mark kennedy said:

Sure but there are so many I can't possibly track them all, yours for instance are off the chart. Here is another string of quotes you cut and paste with very little to say about them:

"You have no idea what I have read or what I know because all you need to know about me is that I'm a YEC and you are immediately considering yourself my intellectual superior

Again, you would not have the slightest idea what I understand and what I don't

This is typical of the two a priori assumptions of Darwinian metaphysics.

First, the a priori assumption of universal common ancestry by exclusively naturalistic causes

If you refuse to make the first assumption then the second one is that you are arguing from incredulity (ignorance).​

These statements reflect an observed pattern in evolutionist remarks and while they apply to many they are certainly not restricted to a certain individual.

That's not the case and the rationalization you are using as a characterature (sic) is more of a performance then a valid criticism. This is how it works, responding to the OP is generally a string of ad hominem attacks undermining any visage of credibility on the part of the creationist. This is usually followed by a series of pedantic and circular questions chosen for the dramatic effect rather then their substantive content. Then enters the scientific type who will cherry pick a few points and if pressed will even make a few substantive points. This individual will be limited to the point made previously by the evolutionists who make the initial contact which is Naraoia's primary difficulty except he is probably not aware of it

Naraoia seems genuinely curious but has picked up on a fallacious thesis

the general attitude of evolutionists like yourself."​

Not a substantive remark regarding a single quote made out of context and offering no real argument contradicting the statements. Her response to them:



Close encounters of the pedantic one liners.



I made no such assumption, that was a conclusion based largely on the genetic divergence and fossil evidence.



You have completely missed the point (or ignored it) that chimpanzee and gorilla ancestors are probably represented in the dozens if not hundreds of fossils uncovered in Africa. Only three teeth represent the chimpanzee ancestors while the Australopithecus and other fossils tend to be better candidates for chimpanzee ancestors then human.



No it's not but since no one every contradicts the ad hominem agitator you can just keep making these rationalizations at random.



You have neither addressed nor seriously examined the many peer reviewed scientific papers that I use as primary source material. Not a single substantive response to them and now you act as if they did not exist in my posts. The data is extensive and user friendly for my purposes since evolutionists never admit a problem for the a priori assumption of universal common ancestry.



My only assumptions are that God is revealed in nature and you are well aware of this whether you admit it or not:

Since what may be known about God is plain to them, because God has made it plain to them. For since the creation of the world God's invisible qualities—his eternal power and divine nature—have been clearly seen, being understood from what has been made, so that men are without excuse.

For although they knew God, they neither glorified him as God nor gave thanks to him, but their thinking became futile and their foolish hearts were darkened. Although they claimed to be wise, they became fools and exchanged the glory of the immortal God for images made to look like mortal man and birds and animals and reptiles. (Romans 1:19-23 New International Version)​

It's not an error to say that every time an ape skull is dug up in Africa it's automatically considered one of our ancestors. For one thing they never consider the possibility that they may well be ancestors of living apes other then humans.



Why you are so self assured of your own credibility speaks volumes for how evolutionists encourage anyone willing to both accept their a priori assumptions and attack creationists.

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I was having a bit of a conversation with you a while back, and next thing I knew you started in on condescending and name calling. Not me, you.

"You are a minion, my dear", specifically.

If you dont like any personal comments then set an example by not doing it, instead of starting it.
You dont seem to like anyone saying anything about your credibility but are awful free about trying to undermine everyone else. Of course, when YOU do it, its ok because its "true". Or so you say.

And of course there is the canard about "everytime and (sic) ape is dug up...." . You modified it a bit at least, but never admitted that you were making a false statement.. Cant admit you were ignoring the apes that have been found in Europe and Asia, as well as the chimp remains from Africa. Guess what? Cant admit a mistake of falsehood=zero respect earned.

I bet you wont admit to the errors Naraoia pointed out, either.

I see this time you added another falsehood about the African apes. Do I need to cut and paste a bunch of references again, to fossil creatures that are considered possibly ancestral to humans AND other apes? Oh yeah, there is also the falsehood about "automatically". They DO look them over, didnt you know?

Care to admit that falsehood, about "automatically". Or you going to stick to it?

If so why should anyone take anything else you say as having any value?

Apologize for the name calling, admit that every word in your claim that every ape fossil is immediately classified as human is false, cut out all the tries to undermine everyone else, and I will not have further comments to make about the quality of your posts. i wont even comment on the English usage.

mark kennedy said:

Again, you would not have the slightest idea what I understand and what I don't.

<stuff>

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True, but you typed this:

"If we were comparing apples to apples and clearly we are not, the substitution, in the open reading frame of a protein coding gene, would most often result in a truncated protein. This is due to a stop codon being inserted causing a frameshift."

While the actual story would be something like...

"An insertion or deletion of a single basepair in an open reading frame causes a frameshift. There are 64 codons (4^3), with 3 of them stop codons. So when assuming that a frameshifted sequence is random, each codon has a ~1/21 chance of being a stop-codon that would prematurely terminate the polypeptide."

Now, I'm willing to believe that you meant to type something like that but didn't for some reason (errors are human etc)

But if you meant to write what you originally wrote, I have to wonder: why should I try to understand your genetics-based-arguments against evolution, when you make large errors while trying to explain very basic genetics?

Mystman said:

True, but you typed this:

"If we were comparing apples to apples and clearly we are not, the substitution, in the open reading frame of a protein coding gene, would most often result in a truncated protein. This is due to a stop codon being inserted causing a frameshift."

While the actual story would be something like...

"An insertion or deletion of a single basepair in an open reading frame causes a frameshift. There are 64 codons (4^3), with 3 of them stop codons. So when assuming that a frameshifted sequence is random, each codon has a ~1/21 chance of being a stop-codon that would prematurely terminate the polypeptide."

Now, I'm willing to believe that you meant to type something like that but didn't for some reason (errors are human etc)

But if you meant to write what you originally wrote, I have to wonder: why should I try to understand your genetics-based-arguments against evolution, when you make large errors while trying to explain very basic genetics?

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Yet another opportunity to acknowledge error, or to dig the credibility
hole deeper.

mark kennedy said:

From the article:

...But the observation of only "one actual kill—and no visual evidence of the spear being used as a spear—weakens it," the University of Southern California (USC) professor said in an email.
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Which is why I said "may".

Primary Sources.

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Thank you. The reason I was puzzled is because so far in this thread, we've been talking about a 94% identity on the level of presence/absence of genes and the widely known 98% identity between comparable sequences, and then you suddenly pulled this 96% out of nowhere. I'm glad to see you actually have a source for it.

Sounds speculative to me and the major morphological changes would have had to start about 2 mya.

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Yes, but our difference is not all morphology. And morphology, though spectacular, is pretty easy to change. I seem to recall from one of these lectures that only 4-5 loci are responsible for the morphological difference between teosinte and maize.

Oh by the way, there is still the matter of ERVs that are found in African Apes but virtually absent in the human genome.

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Are these the ERVs that aren't in orthologous positions in the African apes?

We can do that and also look at some of the other comparisons. I'll probably need to start another tread but it's really no problem. This should help to prime the pump while I get the rest of the detailed specifics together:

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We had a thread about this earlier, and I don't think I ever got a response to my contention (based on someone's analysis of all published hominin cranical capacity measurements as of, I think, 2000) that the change was very neatly gradual, no jumps between species and species. Remember that nice graph with different taxa colour-coded?

I also distinctly remember that I already played around with compound interest in that thread - another thing I don't remember getting a reply to.

Homo habilis that would have lived. 2.5–1.5 mya with a cranial capacity of ~600 cc.

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Range?

The next link would have been Homo erectus with a cranial capacity of ~1000cc.

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Range?

Averages are meaningless without some measure of spread. That's Statistics 101.

It's not 2 million years really, it's closer to half a million years from the rise of Homo habilis to Homo erectus.

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Wa-hait!!! That isn't what we were talking about. We were talking about the tripling of brain size, beginning with the appearance of H. habilis over 2 million years ago, and ending with modern humans (no, the explosion of human brain size didn't stop with H. erectus. And does even H. sapiens actually have an 1500-cc brain on average???)

This is not the same as a near-doubling in 0.5 my.

However, using the same calculator in the same trial-and-error way, I found that doubling cranial capacity in 25 000 generations still only requires a 0.0028% increase each generation (0.0336 cc for a 1200 cc brain). I'm asking again, is that so unbelievable?

You are assuming a smooth linear progression and a successive line,

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I'm assuming exponential increase, not linear (and IIRC, the graph I posted in the earlier thread looks pretty convincingly exponential)

this assumption has hopelessly complicated what is being seen in the fossil record:

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OK, I'm aware that the lineage leading to us is hard to make out in that tangle of branches. However, I think it's now your job to provide a graph similar to this one, with the dubious elements removed. Until you do that, the gradual overall increase still stands.

You are assuming that it is cumulative without deleterious effects.

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I'm assuming that given a selective pressure towards increased brain size, a sufficient number of minorly size-increasing mutations without huge deleterious side-effects arise to respond to it.

But note that the calculation itself says nothing about the genetic change underlying the change of phenotype.

I somehow suspect that you accept that chihuahuas can be bred from wolves, and don't go questioning the genetics.

Only 29% of the genes in the comparison of the Chimpanzee Genome and the Human Genome sequences are the same.

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Now where does THAT come from, and what does "the same" mean? Identical sequence, or what?

More importantly, with brain related genes I have yet to see one that had a beneficial effect.

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Mark, the fact that diseases exist doesn't invalidate the fact that a lot of perfectly normal variation has a genetic (often polygenic) basis. Disease genes get a lot of press, but I seem to recall that other brain-related traits are also getting their share of research nowadays. IIRC a New Scientist feature some time last year mentioned candidate genes in relation to personality, but I'd have to dig around to find the article and/or reference, and I have to go in a few minutes...

No but Schizophrenia, Brain tumors, Alzheimer's disease and Parkinson's disease are devastating disorders.

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And Alzheimer's and Parkinsons usually come out way too late for them to have any influence on the reproductive success of a typical human. Not the best examples

Also, these are major effects that are quite easy to see. The slight variation in brain size that we're talking about is a very subtle effect (and, as I've said, modern human brains vary by orders of magnitude more than needed for the aforementioned tripling)

Gah, I must run now. I'll try to reply to the rest of your post later, but I don't make any promises.

OK, I'm back from training, here comes the remainder...

mark kennedy said:

In Regional Patterns of Gene Expression in Human and Chimpanzee Brains 22&#37; of the genes that showed differences between humans and chimpanzees where due to differences between individuals within their respective species. Gene expression and other normative molecular mechanisms can account for human variation nicely but when it comes to chimpanzee/human divergence it gets more complicated since the differences can be staggering:

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How is a few hundred differentially expressed genes staggering again?

To get some sort of frame of reference, I googled [gene expression disease], and this is the first piece of scientific literature I stumbled upon (Human Molecular Genetics 9:1259).

Huntington's is a single-gene disorder. Yet in the striatum of a mouse model, about 70-100 out of the 6000 assayed genes are misexpressed compared to normal mice.

IOW, genes interact (surprise, surprise... well, maybe not to anyone who's ever had a cursory encounter with developmental genetics). Plus, humans and chimps differ in more genes than transgenic and wild type mice.

Pick a chromosome, any chromosome and you will find a disease or disorder effecting the human brain as the result of a mutation.

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The word is still affecting. (Sorry, grammar/spelling Nazi I am, I know.) Anyway. Pick a chromosome, and you'll probably also find a metabolic disorder, a tumour-related gene and some sort of muscular disorder. You know what? I'll look at all chromosomes for you, 'cause now I'm interested to see if my guess is correct. I'll just pick one example per category per chromosome, 'cause I really don't have the patience to categorise all of them and do statistics. I included approximate directions to find them in the lists.

PLAYTIME!!!

Chromosome 1.

- Metabolic disorder: check (fumarase deficiency, bottom right on the Flash pic).

- Tumour genes: check (what shall I pick? There's loads. B-cell leukaemia will suffice, about 2/3 of the way down the top arm on the right.)

- Muscle disorder: check (congenital muscular dystrophy, 1/3 down the top arm, right)

Chromosome 2, the famous.

- Metabolic disorder: xanthinuria type I, near the top right.

- Tumours: hereditary nonpolyposis colorectal cancer, type I, just under xanthinuria.

- Muscles: another muscular dystrophy and a couple of myopathies, near the bottom right on the short arm.

Chromosome 3.

- Metabolism: sucrose intolerance, near bottom left.

- Tumours: another hereditary nonpolyposis colorectal cancer, near top right

- Muscles: myotonic dystrophy (heaven knows which type, though I wrote part of an essay on them last semester...), near top right of the long arm.

Chromosome 4.

- Metabolism: phenylketonuria, about halfway down the short arm on the left.

- Tumours: acute myeloid leukaemia, bottom left on short arm.

- Muscles: facioscapulohumeral muscuar dystrophy (huh!), near bottom left.

Chromosome 5.

- Metabolism: ketoacidosis, halfway down the short arm on the left.

- Tumours: basal cell carcinoma, near top right of long arm.

- Muscles: autosomal dominant limb-girdle muscular distrophy, not quite halfway down the left of the long arm.

Chromosome 6.

- Metabolism: insulin-dependent diabetes mellitus, halfway down long arm on the left.

- Tumours: acute nonlymphocytic leukaemia, near top right.

- Muscles: congenital merosin-deficient muscular dystrophy, just under diabetes mellitus.

Chromosome 7. (Whee, I found Lunatic fringe Silly gene names rule.)

- Metabolism: trypsinogen deficiency, right at the bottom left.

- Tumours: Ewing sarcoma, top left.

- Muscles: autosomal dominant limb-girdle muscular dystrophy, bottom right of short arm.

Chromosome 8.

- Metabolism: dihydropyrimidinuria, 1/3 way down the long arm on the left.

- Tumours: non-Hodgkin lymphoma, slightly up from dihydropyrimidinuria.

- Muscles: adult onset torsion dystonias, bottom third of the short arm on the right.

Chromosome 9.

- Metabolism: non-ketotic hyperglycinaemia, top left.

- Tumours: sporadic basal cell carcinoma, 1/2 way down long arm, left.

- Muscles: Fukuyama congenital muscular dystrophy, under the carcinoma.

Chromosome 10.

- Metabolism: hyperphenylalaninaemia, top of the long arm, left.

- Tumours: Medullary thyroid carcinoma, bottom third of short arm, left.

- Muscles: autosomal dominant dilated cardiomyopathy, top right of long arm.

Chromosome 11.

- Metabolism: lacticacidaemia, top right of long arm.

- Tumours: Wilms tumour type II, bottom half of short arm, right.

- Muscles: desmin-related cardioskeletal myopathy, bottom half of the part of the list that didn't fit next to the chromosome; right side.

Chromosome 12.

- Metabolism: autosomal dominant hypophosphataemic rickets, near top left.

- Tumours: acute lymphoblastic leukaemia, halfway down short arm, right.

- Muscles: congenital myopathy, halfway down long arm, left.

Chromosome 13.

- Metabolism: hyper[various nitrogen-containing stuff]aemias, a little way below the centromere on the left.

- Tumours: early-onset breast cancer, right next to the centromere on the left.

- Muscles: limb-girdle muscular dystrophy, type 2C, just above breast cancer

Chromosome 14.

- Metabolism: lysinuric protein intolerance, above centromere on left.

- Tumours: T-cell leukaemia/lymphoma, bottom left.

- Muscles: autosomal recessive oculopharyngeal muscular dystrophy, near top right.

Chromosome 15.

- Metabolism (almost typed meatbolism... I think I'm hungry ): hepatic lipase deficiency, halfway down the left.

- Tumours: diffuse large cell lymphoma, top left.

- Muscles: various cardiomyopathies, just above centromere on the right.

Chromosome 16.

- Metabolism: mucopolysaccharidosis, near bottom left.

- Tumours: familiar gastric cancer, some way up from bottom right.

- Muscles: Brody myopathy, bottom half of short arm on the right.

Chromosome 17. (Where we find Radical fringe, another wacky fringe homologue! I wonder if I've missed Manic fringe or it's on a smaller chromosome While we are here, where ARE the hedgehogs??)

- Metabolism: noninsulin-dependent diabetes mellitus, just under centromere on left.

- Tumours: small-cell lung cancer, near bottom left.

- Muscles: myotonia congenita, above lung cancer.

Chromosome 18. (This one doesn't seem to have a lot of anything)

- Metabolism: another insulin-dependent diabetes mellitus (there seem to be loads of genes related to this one), top third of long arm, left.

- Tumours: squamous cell carcinoma, top half of long arm, right.

- Muscles: adult-onset, focal torsion dystonia, near top left.

Chromosome 19.

- Metabolism: type II hypocalciuric hypercalcaemia, fourth from top left.

- Tumours: B-cell leukaemia/lymphoma, bottom right.

- Muscles: muscular dystrophy, fourth from top right.

Chromosome 20. (Cuuute! So tiny! Hmm, I might be getting bored )

- Metabolism: a noninsulin-dependent diabetes mellitus for variety, near bottom of the chromosome on the right.

- Tumours: Rous sarcoma, top third of long arm on the left.

- Muscles: seems I can't find one.

Chromosome 21.

- Metabolism: homocystinuria, halfway down long arm, left.

- Tumours: acute myeloid leukaemia, bottom left.

- Muscles: none I can see.

Chromosome 22. (Ah, HERE is Manic fringe)

- Metabolism: type I hyperprolinaemia, next to centromere on left.

- Tumours: Ewing sarcoma (again... this is another one with a lot of associated loci), a little way down from hyperprolinaemia.

- Muscles: fatal infantile cardioencephalomyopathy (although OMIM says it's a cytochrome c oxidase problem, so it's a bit of an overkill for a muscle disease - but then, myotonic dystrophies aren't all about muscles either), sixth from bottom right.

Chromosome X. (Does that sound ominous. And can you tell I'm getting bored?)

- Metabolism: pyruvate dehydrogenase deficiency, bottom third of short arm, left.

- Tumours: acute myeloid leukaemia, M2 type, near top left.

- Muscles: Duchenne muscular dystrophy, a little way down from the centromere on the right.

And the puny chromosome Y, which has hardly any genes, let alone disease genes...


... Yeah, nothing except a few maleness genes. No brains, no metabolic disorders, no cancers, no muscle disorders, nothing.

The point of this tedious (but fun! Is that a contradiction? ) exercise, if you've managed to scroll this far down:

(1) Saying that some body part or function of a human being has "disease" genes on every chromosome is pretty meaningless, especially without statistics on the level of selective constraint on said "disease" genes. The fact that some mutations in a gene can cause disease doesn't in any way imply that all mutations do.

(2) From the point of view of multiple genetic influences and many ways to go wrong, the brain isn't all that special.

I think we need to take another look at the actual paper

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I think you need to take a look at the Odysseus paper.

Point taken, it has allowed only two substitutions since it's origination 400 mya. That's probably not a substantial or significant point but ok.

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It was just a quibble about accuracy. We're talking science here, after all...

It shows accelerated evolutionary changes in the human lineage, one of the most dramatic anyone has seen so far.

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So does the OdsH homeobox in those flies. But I suppose you don't care who Drosophila simulans has or doesn't have common ancestors with.

I take it you are referring to this paper:

Estimate of the Mutation Rate per Nucleotide in Humans

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Yes, that's the one you took your data from, isn't it?

You seem to have missed the point, if the calculations are based on 1.33% then how do the calculations change is it changes to 5% divergence?

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I might have missed the point because you never stated it, not in this thread at least.

Anyway, let's assume the estimate for mutation rate increases threefold. Now comes the tough question: so what?

Presumably, you don't find a rate of 2.5 &#215; 10[sup]-8[/sup] per site per generation implausibly high, since your argument seems to be that the increased divergence casts doubt on human-chimp common ancestry.

I have to wonder, then, if there never was a 1.33% divergence estimate and these people came up with an overall mutation rate of 7.5 &#215; 10[sup]-8[/sup], would you find that impossibly high? Or is it just a gut reaction of "oh, chimps and humans are more different than we thought, evolution must be bunk"?

mark kennedy said:

Says it all right there, you guys are not shy about making a homology argument but when it comes to the inverse logic your less objective.

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I don't think that's the issue either.

Btw, did you ever address this application of common descent of primates? It's a nice example of why arguing over common descent is so 20th century.

Pete Harcoff said:

I don't think that's the issue either.

Btw, did you ever address this application of common descent of primates? It's a nice example of why arguing over common descent is so 20th century.

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Huh... and here I thought it was so 1st Century.

mark kennedy said:

Oh....my bad.

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Np. From the number of times I've been called a "he" here, most people don't look at the little pink icon. It shouldn't really matter anyway. Science is science, and arguments are arguments, and the value of neither depends on a person's karyotype.

Nice try but I know the difference between a substitution in a nucleotide sequence and a triplet coden interrupted by a change in an amino acid sequence in a protein coding gene resulting in a truncated protein.

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Which is all well, except it's not the difference we were talking about. We are talking about the difference between a substitution and a frame shift. Substitutions don't normally cause frame shifts, yet IIRC you said a truncated protein (i.e., a premature stop) due to a frame shift is their most common outcome.

They don't impress me, as a matter of fact they are wrong so often that I am amazed that an actual scientist would consider them credible.

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Well, I dimly recall one argument in one of the short posts that I thought was dodgy, but by and large, what they say agrees with what I know if I know something about the subject, and I don't remember any glaring errors of reasoning apart from that one bit I once noted (and I should go back to check if it really is dodgy). And, again, the FAQs/essays tend to cite tons of primary sources where you can check the evidence.

That might make sense to you but it entirely too general after the detailed specifics I offered you.

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Which "detailed specifics" are you talking about? I was referring to your odd substitution/frame shift confusion, nothing else.

A conclusion made before there was such a thing as genetics, molecular biology or modern paleontology.

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And strangely enough, most geneticists, molecular biologists and palaeontologists think their field strengthens it.

Yea I can tell since you have less and less interest in it.

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And what does that remark even mean?

No it's easy, you quote what they said, make the correction, cite the source and move on. What other people say is only important when you are depending on a mob psychology to affirm your position.

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And again, you are making an argument from the number of times a point is made rather than the merits of the point. Being popular doesn't make an argument right, but it equally doesn't make it wrong.

Gosh, are we really arguing about my entirely subjective decisions to reiterate or not reiterate a point?

You have gotten to the point where you are ignoring every substantive and scientific point and talking in vague generalities.

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What substantive scientific point is there in this?
This is the paragraph I responded to. Once again, there is not a single concrete example, and not a single trace of scientific information here, so I don't know why responding with a general and non-scientific opinion means that I'm ignoring all of your substantive, scientific points.

Trust me and the real world comparisons that 98% is just plain wrong.

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I'm perfectly happy to trust you after you've cited trustworthy sources and made it clear what kind of similarity you're talking about. As I said, I don't have any particular attachment to that number.

It compares the nucleotide sequence of humans and chimpanzees. Now, when it comes to whole genomes being compared it did not happen until the Chimpanzee Consortium finally released it's initial sequence but even then it was about 95%.

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Fine with me.

See I have correctly bolded the parts that account for the indels (gaps)

the overall sequence difference was estimated to be approximately 5% by taking regions of insertions or deletions (indels) into account.

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Yup, I saw that. But the 98% estimate didn't include indels, at least not the 98% estimate mentioned in that paper. 1.23%-2% divergence was estimated for substitutions in aligned sequences by earlier studies, and for the same measure of divergence, these authors came up with 1.44%. No, this is not the overall divergence, all mutations included.

I think we can agree on that and move on now.

Which are, gross structural changes affecting gene products are far more common than previously, an estimated 20.3% of the PTR22 proteins

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Far more common than previously thought, you mean? Yes, but what is the significance of that? If our small amount of sequence divergence translates to relatively big differences in the products, it only becomes easier to reconcile the levels of genetic and phenotypic difference between humans and chimps.

we compared the gene expression profiles of HSA21q genes between humans and chimpanzees in two tissues: 202 genes in brain (cingulate cortex, HG U95Av2, B, C, D and E) and 96 genes in liver (HG U95Av2). We detected 60 genes expressed in brain (this study) and 40 in liver41 in at least one species. Of these, 9 in the brain and 12 in the liver showed a significant change in expression level between humans and chimpanzees in the range of a 1.5–10-fold difference

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Where does gene expression come into this? I thought we were talking about sequence divergence??

Furthermore, what are you trying to argue with these expression data? (I don't know if you addressed the mouse Huntington's expression data in another post, so don't respond if you already did.)

That know divergence has grown to include the many genes that have been gained and lost. Now the statistics make it more like 96% and you have completely missed that point or ignored it.

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I didn't miss it (remember, that's where I went with the "mob" and pointed out that gene gain/loss differences can't be compared with nucleotide-level differences). I thought the discussion has drifted away from the duplication/loss study long ago, but if you really want to return to it, go ahead.

Congratulations! You have managed to side step every single peer reviewed article on the subject except for one.

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I'm not sure what you're referring to. Care to elaborate?

This seems a common communication problem with you. I say something about data you use or an argument you make, and then you reply with something that doesn't directly address what I wrote and doesn't make it clear what (if anything) it does address. Maybe it's just me, or maybe it's you having problems conveying your point.

Naraoia said:

Np. From the number of times I've been called a "he" here, most people don't look at the little pink icon. It shouldn't really matter anyway. Science is science, and arguments are arguments, and the value of neither depends on a person's karyotype.

Which is all well, except it's not the difference we were talking about. We are talking about the difference between a substitution and a frame shift. Substitutions don't normally cause frame shifts, yet IIRC you said a truncated protein (i.e., a premature stop) due to a frame shift is their most common outcome.

Well, I dimly recall one argument in one of the short posts that I thought was dodgy, but by and large, what they say agrees with what I know if I know something about the subject, and I don't remember any glaring errors of reasoning apart from that one bit I once noted (and I should go back to check if it really is dodgy). And, again, the FAQs/essays tend to cite tons of primary sources where you can check the evidence.

Which "detailed specifics" are you talking about? I was referring to your odd substitution/frame shift confusion, nothing else.

And strangely enough, most geneticists, molecular biologists and palaeontologists think their field strengthens it.

And what does that remark even mean?

And again, you are making an argument from the number of times a point is made rather than the merits of the point. Being popular doesn't make an argument right, but it equally doesn't make it wrong.

Gosh, are we really arguing about my entirely subjective decisions to reiterate or not reiterate a point?

What substantive scientific point is there in this?This is the paragraph I responded to. Once again, there is not a single concrete example, and not a single trace of scientific information here, so I don't know why responding with a general and non-scientific opinion means that I'm ignoring all of your substantive, scientific points.

I'm perfectly happy to trust you after you've cited trustworthy sources and made it clear what kind of similarity you're talking about. As I said, I don't have any particular attachment to that number.

Fine with me.

Yup, I saw that. But the 98% estimate didn't include indels, at least not the 98% estimate mentioned in that paper. 1.23%-2% divergence was estimated for substitutions in aligned sequences by earlier studies, and for the same measure of divergence, these authors came up with 1.44%. No, this is not the overall divergence, all mutations included.

I think we can agree on that and move on now.

Far more common than previously thought, you mean? Yes, but what is the significance of that? If our small amount of sequence divergence translates to relatively big differences in the products, it only becomes easier to reconcile the levels of genetic and phenotypic difference between humans and chimps.

Where does gene expression come into this? I thought we were talking about sequence divergence??

Furthermore, what are you trying to argue with these expression data? (I don't know if you addressed the mouse Huntington's expression data in another post, so don't respond if you already did.)

I didn't miss it (remember, that's where I went with the "mob" and pointed out that gene gain/loss differences can't be compared with nucleotide-level differences). I thought the discussion has drifted away from the duplication/loss study long ago, but if you really want to return to it, go ahead.

I'm not sure what you're referring to. Care to elaborate?

This seems a common communication problem with you. I say something about data you use or an argument you make, and then you reply with something that doesn't directly address what I wrote and doesn't make it clear what (if anything) it does address. Maybe it's just me, or maybe it's you having problems conveying your point.

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I am going to bow out on making comments in the thread, for one reason that I never did care much for genetics.

Couple of comments tho. Since I am not looking at the details of the genetics discussion maybe some other aspects are more clear to me.

Most obvious is that the reason for what looks like a communication problem is that this is not a fair and honest discussion.

One, is that mk makes fallacious assertions, and will take no responsibility to correct, acknowledge, or stop doing it.

Another is that he is, as he has stated, coming from a mind set, paradigm if you like, that all scientists are hopelessly biased and incapable of ever doing objective work.

By the same token, (as he stated) no creationist can-.he says- ever get published and no matter how valid their work is, it will be ignored because it is from that source and they dont buy into the great a priori assumption of the evos.

Also that human being are not apes, that they are a special creation and that this is Truth.

Basically you seem to be arguing against the Truth of the Bible, but talking about genetics.



If that is worth discussing, it would still be a much cleaner discussion if it stayed on topic, with a moratorium on all the dissertations on the perceived personal qualities of others.

as in-

"That's not the case and the rationalization you are using as a characterature is more of a performance then a valid criticism. This is how it works, responding to the OP is generally a string of ad hominem attacks undermining any visage of credibility on the part of the creationist. This is usually followed by a series of pedantic and circular questions chosen for the dramatic effect rather then their substantive content. Then enters the scientific type who will cherry pick a few points and if pressed will even make a few substantive points. This individual will be limited to the point made previously by the evolutionists who make the initial contact which is Naraoia's primary difficulty except he is probably not aware of it."

mark kennedy said:

So you have completely forgotten the OP and the paper this thread is based on I see.

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Didn't that paper estimate a 6% difference, which would mean 94% identity, not 96%?

Interesting...your point?

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That even though most of the morphological change is crammed into the last third of our lineage, the same need not be the case for the genetic change.

Just the ERVs in general, not just comparing the ones known to be the same.

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You might want to refresh my memory, then. It's a bit patchy on ERVs.

I have no idea what you are talking about or why you have ignored the carefully prepared and detailed measurements of the various skulls.

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Carefully prepared and detailed measurements of the various skulls?

The dataset in this study is a carefully prepared and detailed measurement. Of not just a few skulls, but hundreds of them belonging to diverse hominin taxa, all the way from 3.2 Mya to 10 000 years ago. Note this, from the summary:

De Miguel & Henneberg 2001 said:

When hominid CC by taxon with date as a covariate is subjected to ANOVA, taxon is responsible for 5% of the variance while date is responsible for the main portion, (89%). The relationship between CC and date is best characterised as a gradual time trend. It is proven by the ANOVA test for linearity, by G test for trend and by ASReml fitting of a linear function. The line of best fit to this time trend is a double exponential curve which explains 90% of the total variance in CC:

CC = 306.63 (4.83[sup]0.9995[sup]DATE[/sup][/sup])

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(My eyeball guess of an exponential curve, based on Nick Matzke's colour-coded rendition, was wrong, the trend is double exponential.)

Key point to note: taxon accounts for only a tiny amount of variation - when the creature lived matters more than where it falls taxonomically. Now there might be an issue with specimens of uncertain affinities, but I wouldn't think it's so large that it could reverse the relative explanatory power of age and taxon (maybe a separate coding for H. erectus and ergaster would be useful, though; while I'm not aware of a major difference in their distribution of cranial capacities, that doesn't mean there isn't a difference).

Anyway, this could easily mean that whatever the precise lineage of H. sapiens is, a similar time trend applies to it.

If you say so.

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Great, way to address a point!

Do you accept that averages on their own mean sod all, or do you not? If not, why? If yes, please stop giving me average cranial capacities as if they were a better indicator of trends than a detailed data set of two and a half hundred individual skulls.

I thought you were a biologist that understood that a molecular basis was crucial.

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I am a not-yet-biologist, and I understand that you can study natural selection without looking at DNA.

It's a nice bonus if you find the genetic culprit for a particular change - but it is rather difficult if the change is in a massively polygenic trait that's difficult to experiment on... you don't genetically manipulate humans just to study how a gene affects their brain development.

It sucks if it turns out that you can't explain the change with genetics - but again, the change being in a trait under highly complicated genetic influences, it's not so easy to say whether you can or can't explain it!

Overall, though, if you observe that certain changes can occur under selection, you'd be daft to declare that they can't just because you don't know what's going on at the molecular level.

Granted, I haven't heard of an example of observed evolution in brain size in particular, but there are plenty of examples of selection at work. Chihuahuas I brought up because they are a spectacular and "condensed" example. Very different from their wolf ancestors (both morphologically and behaviourally, I think), but this difference was achieved entirely without knowledge of the underlying genetics, let alone conscious genetic manipulation. And whatever genes did it, it clearly worked.

As for the human brain, again, variation within modern humans is orders of magnitude larger than what would be required to get from australopiths to us in three, two or even half a million years. All you need to do is chop off the lower tail of the distribution in each generation, and so long as there are brain size-affecting mutations, the average will keep creeping upwards.

Sure, that only takes into account brain size, but are the differences between human and other ape brains really qualitative, or are they just differences of degree? (New cell types? New structures that are organised in novel ways? Or is it just extra lumps of the old cells and a little more cell adhesion?)

When you are talking about 18 substations in a regulatory gene that is only 118 nucleotides long and has not allowed more then two in 400 million years it is.

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No, a tripling in 2 my never is the same as a doubling in 0.5 my. You shifted the goalposts and now you try to weasel out of it by bringing in a completely different argument.

Which, by the way, is fallacious if you are hung up on the contrast between the long conservation and the rapid divergence of HAR1, because that would only be odd if the selection on HAR1 was constant over the whole time period in question.

First you want to be touchy about how we do the statistics and then you want to talk in generalities. Typical.

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How is a concrete experiment based on your specifications "generalities"?

How about a real comparison:

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Listing unqualified average values from arbitrarily chosen species counts as a real comparison as opposed to a dataset of all published measurements of hominin skulls between 10 000 and 3.2 million years of age?

I assume you realize that natural selection cannot account for the actual divergence:

There is tentative evidence from in-depth analysis of divergence and diversity that natural selection is not the major contributor to the large-scale patterns of genetic variability in humans Nature 437, 69-87 (1 September 2005)

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I assume you realise that what you quote says no such thing?

The quote (which, in fact, cites the conclusions of other papers) apparently refers to patterns of variation across different regions of the genome within the human species. Presumably, if natural selection is not the major contributor, it's drift...

*checks citations*

Ow, differential mutation rate, it seems. Both studies cited there (Hellmann et al. 2003 and Lercher & Hurst 2002) investigate the influence of local recombination rates on diversity in particular genomic regions, and the first one concludes that "regions that experience less recombination have reduced divergence to chimpanzee and to baboon, as well as lower levels of diversity. This observation suggests that mutation and recombination are associated processes in humans, so that the positive correlation between diversity and recombination may have a purely neutral explanation."

The paragraph also doesn't discuss whether selection can explain divergence per se, but the regional variation in divergence. As to that, they conclude that regional variation in mutation rates is probably a better explanation.

How does that undermine human-chimp common ancestry again?

I don't think that's actually a problem but artificial insemination could prove that one way or the other. There are a lot of cross overs and bottle necks involved, it's hard to say.

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I see. So why do you question the genetic basis of selection when it comes to your own species? Do I smell double standards?

Just a mean average, I didn't expect you to follow.

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How flattering of you. Just so we're clear about my meaning:

"Where does that come from" means "what's your source". If one of your earlier references contained that estimate, I missed it.

"What does 'the same' mean" means... what it says. Is it the same at orthologous positions, same as in no substitutions or indels, same as in has an orthologue in the other species... what? I thought you realised by now that there are two many kinds of similarity and difference for you to be able to simply say "the same" and expect everyone to understand what you mean. That's asking us to read your mind.

With that in mind, do you want to give it another go?

Dear trust me when I say, its not worth worrying about. You wont find any.

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Way to be scientific, there.

It's not important anyway even though I have gotten a lot of millage out of that particular argument evolutionists have no answer for.

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Can anyone help me translate this sentence?

Just listen to me one time, that is all I ask. I want to know what makes butterflies, birds and arctic wildlife adapt to changing conditions.

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You read scientific literature, don't you? Have you tried anything other than human/chimp genetics? I'm sure there is a lot out there that could help you.

I can't give you concrete studies off the top of my head, but one specific example that's quite well-known is Pitx1 enhancer evolution and pelvic spine size in sticklebacks. I think there was also a genetic study of the famous beak of the famous finch a while ago. I've already mentioned teosinte and maize, though I can't remember if anyone looked at the actual loci or just estimated how many there are.

And then there's the textbook example of sickle-cell trait and its heterozygous advantage.

If you've seen all of this before, then give me some time and I could try to dig up something more obscure... though I don't think I know any more papers on the genetics of adaptation than you do.

Wait!

I think I can give you a precise citation, and it was your mentioning Arctic wildlife that reminded me of that. Here is one on the way lactate dehydrogenase adapted to functioning in extreme cold in Antarctic fish:

Fields PA, Somero GN (1998) Hot spots in cold adaptation: Localized increases in conformational flexibility in lactate dehydrogenase A4 orthologs of Antarctic notothenioid fishes. PNAS 95:11476-11481

Adaptation, check, molecular mechanism, check.

I want to know what those molecular mechanisms are, even if it's speculative. That is the only reason I continue to pursue these discussions because every great once in a while I find another piece of the puzzle.

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That's a worthy goal.

They are the effects of mutations on the human brain right?

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Yes (though IIRC in both cases, a "disease allele" is only a risk factor), and if their only negative effect manifests long after humans typically stop reproducing, they aren't truly deleterious in the evolutionary sense.

Argh, I so want to just take one of MK's posts and do a long detailed rebuttal of it. His stuff is almost as good as RB's statement that metatherian mammals hyperevolved from their eutherian "counterparts" to repopulate the world after the Flood.
I'll do it later this week when I have a day off.

BananaSlug said:

Argh, I so want to just take one of MK's posts and do a long detailed rebuttal of it. His stuff is almost as good as RB's statement that metatherian mammals hyperevolved from their eutherian "counterparts" to repopulate the world after the Flood.
I'll do it later this week when I have a day off.

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Please do. I have about a million deadlines and then exams coming up, and I really shouldn't be procrastinating on CF before the end of May.

(Of course, I will keep procrastinating, whatever I say about deadlines, but it would still be nice to have someone else willing to dissect long posts )

mark kennedy said:

Naraoia,

Forgive me but I am in the middle of a move and I am unable to respond to your posts as I want to. I find you responses as entertaining as I find them challenging and I assure you I will be responding as soon as I am able.

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Don't worry. In fact I'm relieved that I'll have time to do other things besides posting in this thread )

For some reason woman make great biologists and seem to have a real talent for genetics.

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And all generalisations are false

By the way, I found the New Scientist feature on personality. The article is here, but it needs subscription, so relevant part quoted:

New Scientist said:

For example, there are two common forms of the serotonin transporter gene which codes for the substance that removes the mood-affecting neurotransmitter serotonin from the gaps between neurons. People with at least one copy of the short form of the gene have higher neuroticism scores than people with two copies of the long form. The genetic findings also correlate with the neuroscientific ones. In the brain scanner, individuals with one or more short forms of the gene show a greater spike of amygdala activity when they are presented with a fearful face than do individuals with two long forms.

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It seems that an earlier article (13 September 2003) covered this in more detail, and it mentions another example, a dopamine receptor whose alleles correlate with extroversion.

If you are interested, I hunted down papers:

Lesch KP et al. (1996) Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region. Science 274:1527-1531

(However, I looked at the related links on PubMed, and found some controversy. This study didn't find an association, this one did. So it seems you need detailed reading to make up your mind about this example.)

Ebstein RP et al. (1996) Dopamine D4 receptor (D4DR) exon III polymorphism associated with the human personality trait of Novelty Seeking. Nature Genetics 12:78-80

and

Benjamin J et al. (1996) Population and familial association between the D4 dopamine receptor gene and measures of Novelty Seeking. Nature Genetics 12:81&#8722;84

In all fairness, the 2003 New Scientist article mentions that later meta-analyses (for example, here) of these studies found the evidence to be wanting - but also that newer research does support an association of certain loci with neuroticism scores...

Naraoia said:

In all fairness, the 2003 New Scientist article mentions that later meta-analyses (for example, here) of these studies found the evidence to be wanting - but also that newer research does support an association of certain loci with neuroticism scores...

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Association studies of genes with complex traits had a miserable rate of successful replication (see Genet Med. 2002 Mar-Apr;4(2):45-61 for the situation with disease association studies). It's reasonable to assume that most such reports were wrong. (This is no longer the case, with the advent of whole genome association studies, but it was true when these studies were done.)

Thanks. It did seem like a horribly messy subject even at a brief glance...