Creationism and Human Brain evolution

[Pete Harcoff]

There is even some speculation that retroviral inserts provide some input for "major divergance" in the form of non-essential DNA sequences. (I personally think that this is unnecessary, even if possible).

Heh, then don't ever read the novel, "Darwin's Radio".

 

[mark kennedy]

Considering I doubt you actually took the time and resources to actually look up the citations, I find your conclusion a little underwelming.

I also find it odd that you'd call a protrusion from the base of the lower back complete with vertebrae something that just "resembles a tail". Exactly what do you think a tail is?

I honestly have no idea but the article on the two genes you mentioned discussed the resemblance of the genes in the two geomones. It was speculated that mutations had something to do with humans losing their tails but that was it. Then there was the x-ray of the girls tail that was cited as coming from a Pub Med article that reported on it but all I have seen is the x-ray and the abstract.

Look Pete, genes are linked across chromosomes and the rule of thumb is the farther away they are the more often they recombine. Let's say somehow these genes are involved in monkey tail development and the gene somehow either gets the right combination or the nucleotides that have been deleted (I did find a comparison of mouse and human samples of them btw, the human counterpart was 61%). This does not account for the effect of the gene change on recombination.

It's an interesting argument but even with the vertebrae I am not convinced that we are looking at a monkey tail on a human. You cut and pasted a section of an article that led me on a dead end. One of these days if I think of it I will look up the article in Pub Med at the library but I wont be doing that tonight.

You never said what you thought of the OP. What did you think of the differences in the gene sequences? I thought the differences between individules within the respective species was fascinating myself. They threw the diversity estimates of the researchers off by 22%.

 

[mark kennedy]

Well, I guess that settles that. It seems real science does not stand a chance when you have an internet connection and 15 minutes to spare.

I admit that it does not settle much but it was a dead end argument unless the genes and the abnormality on that girl can be connected.

 

[Dr.GH]

I would like to read that reference please. And what is the problem of major diverance to evolutionary theory? OH MY WHATEVER is that creato "macroevolution?" That is certainly one favored form of speciation. There is even some speculation that retroviral inserts provide some input for "major divergance" in the form of non-essential DNA sequences. (I personally think that this is unnecessary, even if possible).

Let's look at the whole quote:

Endogenous retroviruses.

Endogenous retroviruses (ERVs) have become all but extinct in the human lineage, with only a single retrovirus (human endogenous retrovirus K (HERV-K)) still active24. HERV-K was found to be active in both lineages, with at least 73 human-specific insertions (7 full length and 66 solo long terminal repeats (LTRs)) and at least 45 chimpanzee-specific insertions (1 full length and 44 solo LTRs). A few other ERV classes persisted in the human genome beyond the human−chimpanzee split, leaving

9 human-specific insertions (all solo LTRs, including five HERV9 elements) before dying out.

Against this background, it was surprising to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2) that are unlike any older elements in either genome; these must have been introduced by infection of the chimpanzee germ line. The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (

5−8) invasions, because the sequence differences among reconstructed subfamilies are too great (

8%) to have arisen by mutation since divergence from human. It is closely related to a baboon endogenous retrovirus (BaEV, 88% ORF2 product identity) and a feline endogenous virus (ECE-1, 86% ORF2 product identity). The larger family (PtERV1) is more homogeneous and has over 200 copies. Whereas older ERVs, like HERV-K, are primarily represented by solo LTRs resulting from LTR−LTR recombination, more than half of the PtERV1 copies are still full length, probably reflecting the young age of the elements. PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon, suggesting separate germline invasions in these species68.

In short, the ERVs I have cited are famlies in the sense that they were viral DNA with some degree of variability that after insertion into the genome of their primate hosts, began to further viverge.

 

[mark kennedy]

Let's look at the whole quote:


In short, the ERVs I have cited are famlies in the sense that they were viral DNA with some degree of variability that after insertion into the genome of their primate hosts, began to further viverge.

I quess I never really got the signifigance of the retrovirus. I allways thought it just made its way into the human germline the same way it did in the apes. The fact that we were effected by one and they were effected by several others never really peaked my attention.

I read the section in the article and went through yours as best I could. Call it an argument from incedulity, I just don't attach any real signifigance to this retrovirus.

 

[Dr.GH]

I read the section in the article and went through yours as best I could. Call it an argument from incedulity, I just don't attach any real signifigance to this retrovirus.

Mark, It is not just a single retrovirus, it is thousands. And there is not just one sort of retovirus, there are many families of retorvirususes. Further, entire lineages, each with their own heritage of retroviral DNA, and become extinct, and those DNA sequences have disappeared.

 

[ushishir]

Jianzhi Zhang tried to determine if positive selection of amino acid substitutions that left the reading frame open are detectable in the ASPM gene. He instead found strong purifying selection and concluded that the postive selection of the ASPM gene took place time between 6–7 and 0.1 MY ago (0.5 x 10,000 generations x 20 years/generation). Researchers have determined that the gene is still evolving but I wonder how a congenital developmental defect characterized by severely reduced brain size could be an advantage.

The positively selected mutations are obviously not those that cause severly reduced brain size. Some mutations in ASPM cause severly reduced brain size - usually those resulting in a truncated protein (see OMIM) - the ancient and recent positively selected mutations do not. In europe the selected variant (containing 2 nonsynonymous substitutions) is present in about 40% of individuals, last time i checked 40% of europeans did not have 'severely reduced brain size '. To conflate disease causing mutations with those that are neutral or beneficial utterly wrong, and perplexing as it is completely illogical.

 

[Loudmouth]

I quess I never really got the signifigance of the retrovirus. I allways thought it just made its way into the human germline the same way it did in the apes. The fact that we were effected by one and they were effected by several others never really peaked my attention.

Of course you haven't, because it destroys the idea of separate lineages.

These viruses do act alike in all apes (including humans). They randomly insert amongst thousands of integration sights. Let's say that there are 2,000 insertion sights for Virus A (HIV has over 5,000 so this is being generous). The chances of two individuals sharing the same insertion in the same spot in their genome is 1 in 2,000. The odds of an entire population of 1 million individuals sharing the same insertion through separate infections is astronomical, so it is safe to say that a common insertion across and entire population is due to a single infection in a single individual and that insertion was then fixed in the population. However, we are not talking about one insertion that is the same amongst all in the population, we are talking about hundreds. On top of that, we share a lot of those insertions with other primate species. These shared insertions can not be explained through separate infections, only through common ancestory.

I read the section in the article and went through yours as best I could. Call it an argument from incedulity, I just don't attach any real signifigance to this retrovirus.

Of course you don't. The reason is quite obvious. ERV's are very inconvenient evidence for your claims so it must be ignored and discredited.

 

[TeddyKGB]

These viruses do act alike in all apes (including humans). They randomly insert amongst thousands of integration sights. Let's say that there are 2,000 insertion sights for Virus A (HIV has over 5,000 so this is being generous). The chances of two individuals sharing the same insertion in the same spot in their genome is 1 in 2,000.

That can't be right. It has to be much worse than 1 in 2000. I am just too sick to think right now.

 

[Loudmouth]

That can't be right. It has to be much worse than 1 in 2000. I am just too sick to think right now.

I was being generous. Hope you feel better soon.

 

[Loudmouth]

[Human brain development] is unprecedented in it's scope, effect and size.

No it is not. I would contend that the whale lineage went through a much more unprecedented change than the human lineage.

What's more we have the comparative samples right in from of us.

We do? I thought you said they were myths?

Afraid you can't do that with reptile growing feathers and turning into a bird.

Actually, birds are classified as reptiles, or more specifically as dinosaurs.

The divergance between dogs is not that great and it is possible when you take into consideration transposable elements, transcript factors and recombination of genes during meiosis.

I would argue that there is more morphological divergence between a St. Bernard and a Chihuahua than there is between a human and a chimp.

Why not explore the only alternative to the single common ancestor model? Seperate lineage.

The single common ancestor model is falsified by the evidence. Why should I consider a falsified model?

 

[ChrisPelletier]

The single common ancestor model is falsified by the evidence. Why should I consider a falsified model?

It has?

 

[Dr.GH]

Quote

Why not explore the only alternative to the single common ancestor model? Seperate lineage.

The single common ancestor model is falsified by the evidence. Why should I consider a falsified model?

I am confussed here as well. The notion of common ancestor has not failed, unless you are refering to the notion that this is a single unique individual. And then I would agree, because evolution is a process of populations over generations, and not just a singe unique instance when a new species bursts into existance in the form of a single individual.

The notion of seperate lineages was the principle model used in the 1700s and early 1800s. Simply, it failed to be able to account for the observable fossil data. The notion of punctuated equilibria is not a rejection of common decent, or even gradual change. Had there been any data supporting seperate creation, or the naturalistic version called "saltationism" it would be the standard theory. But nature didn't make huge leaps, and the fossil record does not have the instant appearence of totally unique organisms, even at the phyla level of classification, even at the early Cambrian. [url="http://www.pandasthumb.org/archives/2004/08/meyers_hopeless_monster.html"]Meyer’s Hopeless Monster[/url] is a through debunking of the Cambrian "explosion" as a creationist icon.

 

[Pete Harcoff]

I honestly have no idea but the article on the two genes you mentioned discussed the resemblance of the genes in the two geomones. It was speculated that mutations had something to do with humans losing their tails but that was it. Then there was the x-ray of the girls tail that was cited as coming from a Pub Med article that reported on it but all I have seen is the x-ray and the abstract.

Well, there was also the bit about human tail growth during development. Fact is, we do develop tails, but they don't completely develop which is why we are left with little more than a coccyx.

It's an interesting argument but even with the vertebrae I am not convinced that we are looking at a monkey tail on a human.

Of course it's not a monkey tail. It's a human tail! That's the whole point. We have genes to develop tails in our genome and even begin developing them in the embryonic stage. Yet, for some reason we lose those tails during development.

You cut and pasted a section of an article that led me on a dead end. One of these days if I think of it I will look up the article in Pub Med at the library but I wont be doing that tonight.

I think you should go back and read more, particularly the section on embryonic tail development (it's a bit below the section on atavistic tails). In fact, I think you should just read the entire FAQ, since it nicely sums up some of the evidence which leads scientists to conclude common descent in the first place. After all, if you're going to argue against it, you should at least familiarize yourself with the evidence.

Also, the refs are in PubMed, but they're not all online. I know at my Uni they don't even have the appropriate journals (not surprising since they are medical case reports), so it might be tough to find the originals. Even so, the abstrate for this case report is telling:

A case of a tail in a 2-week-old infant is reported, and findings from a review of 33 previously reported cases of true tails and pseudotails are summarized. The true, or persistent, vestigial tail of humans arises from the most distal remnant of the embryonic tail. It contains adipose and connective tissue, central bundles of striated muscle, blood vessels, and nerves and is covered by skin. Bone, cartilage, notochord, and spinal cord are lacking. The true tail arises by retention of structures found normally in fetal development. It may be as long as 13 cm, can move and contract, and occurs twice as often in males as in females.

So if you're trying to argue it's something other than a human tail... Well, I just don't see it. If it walks, talks and quacks like a duck...

And yeah, I'll eventually get to the OP. I just was initially responding to what others had written in this thread...

 

[sfs]

Higher recombination can improve fittness by providing more alleles but you are talking about a deletion event. This kind of an indel can be neutral in some cases but the real trick is keeping the reading frame open. Chances it would get out of the transcription check point or be eliminated by genetic drift. The only way of establishing it in the genome is for it to provide a selective advatage. On average the rate would be 3 to 7 nucleotides being established on average for millions of years.

I'm afraid this paragraph looks like a string of words thrown together without any regard to meaning. A few points: an indel only has to keep the reading frame open if it occurs in the coding region of a gene. 98% of indels will occur elsewhere, so there is no reading frame to worry about. Of the 2%, 2/3rds will disrupt the reading frame and very likely be eliminated as deleterious. Why are you even talking about these events? Just how many indels within reading frames do you think there are between humans and chimps? Most indels occur in nonfunctional parts of the genome, so no selection is involved.

 

[sfs]

Now, getting to your point. What happens when these plants and animals are breeded for desired traits is genes recombine during meiosis. Certain traits that are recessive (your favorable traits) but when breeded hybrids can have a higher frequency and thus become dominant. The real problem with this is that there is a strong tendancy of the frequency to revert back to the original wild type. Also when these hybrids are breeded for a while they get a genetic bottleneck from inbreeding.

I'm afraid this is thoroughly confused. Recombination mixes up genes that were on the same chromosome in the parent; it permits lots of gene combinations to be tried. Traits desired by breeders may be recessive or dominant or neither; frequency has nothing to do with it. The traits the breeders want can usually be produced by selecting from existing genetic variation, but sometimes breeders do have to rely on new mutations to provide the trait they want.

 

[mark kennedy]

So if you're trying to argue it's something other than a human tail... Well, I just don't see it. If it walks, talks and quacks like a duck...

And yeah, I'll eventually get to the OP. I just was initially responding to what others had written in this thread...

I'm not really dismissing it, I have no idea what this appendage is. I don't really trust Talk Origins and until I see the Pub Med article I'm not sure what this is supposed to be. By the way, I read the FAQ and everything they had on it. However, the connection to these genes you mentioned doesn't seem clear. I'll let you know if I can track down any of the papers they cited.

 

[mark kennedy]

I'm afraid this paragraph looks like a string of words thrown together without any regard to meaning. A few points: an indel only has to keep the reading frame open if it occurs in the coding region of a gene. 98% of indels will occur elsewhere, so there is no reading frame to worry about. Of the 2%, 2/3rds will disrupt the reading frame and very likely be eliminated as deleterious. Why are you even talking about these events? Just how many indels within reading frames do you think there are between humans and chimps? Most indels occur in nonfunctional parts of the genome, so no selection is involved.

Of course most of the indels will appear in the nonfuctional parts of the genome, theres less selective pressure there. In the Chimpanzee Chromosome 22 paper they identified gross structural changes in the protein coding genes, 15 in fact, which got me thinking about this. I'm still not sure what kind of indels there are in other chromosomes but I was pointing out that keeping the reading frame open was crucial when there was any change in the amino acid seqeunce.

 

[mark kennedy]

I'm afraid this is thoroughly confused. Recombination mixes up genes that were on the same chromosome in the parent; it permits lots of gene combinations to be tried. Traits desired by breeders may be recessive or dominant or neither; frequency has nothing to do with it. The traits the breeders want can usually be produced by selecting from existing genetic variation, but sometimes breeders do have to rely on new mutations to provide the trait they want.

I was making some passing remarks comparing artificial selection to natural selection. When you get more recombinations then you will get more alleles, at least there's a better chance. I'm not real clear what you mean by mutations here but from what I gather sometimes there are mutations in the genes controling smell, hair color...etc. I'm not really sure how much of this is an actual mutation and what other factors might be at work. I suspect things like transcript factors, turning genes on and off or something along those lines are part of it. One of the problems with domesticating wild animals is they they tend not to breed or produce infertile offspring. I expect there are very simular problems with mutations depending on where they show up.

 

[mark kennedy]

Just a reminder, the original intention of the thread was to ask these questions. There is a tendancy to run off on tangents and I am as quilty as anyone but this is what I had in mind when writting the essay in the OP:

I bring you yet another renunciation of the much celebrated, never demonstrated, often pontificated, single common ancestor model...but seriously folks. Let us ponder the the most signifigant questions confronting the single common ancestor model in our day. What makes us human? (Nature 437, 69-87 ) What is the genetic basis for the threefold expansion of the human brain in 2 1/2 million years?(Genetics, Vol. 165, 2063-2070) What is the genetic and evolutionary background of phenotypic traits that set humans apart from our closest evolutionary relatives, the chimpanzees?(Genome Research 14:1462-1473)