Biology Prof: Evolution Isn’t Theory, it’s Fact

Human Events ^ | August 17 | Christopher Flickinger

[Right Wing Professor]

However, this phenotypical diversity is limited by the genotypic pool and dogs in all their wonderful variety do not give rise to cabbage in one or one million generations.

You have no idea what dogs could give rise to in a million generations. We've only been playing with them for a few hundred. And in that time, we've produced something that's convergently evolved with a tailless rat (chihuahuas). (You can tell I don't like chichuahuas). A dog won't give a cabbage in a million generations, but it could, IMO, give rsie to something we'd be inclined to class in an entirely different family, if we didn't know its origin.

Also, dog diversity is not limited by the pre-existing genotypic pool. It made good use of mutation.

[Diamond]

...then one would expect to find that particular infection events would occur in the target species with a random frequency unrelated to the presumed common ancestry of various species.

No, I'm suggesting the possibility of an enzymatic mechanism for the insertion locations as opposed to nonfunctional products of retroviral infection that have inserted randomly into the host. The whole proof of the common descent explanation lies in the vast improbability of mostly random viral insertions occurring in the same location in two different mammalian species because the DNA chain is too long for coincidence.

Cordially,

[narby]

I suppose I was foolish to imagine that you'd take a summary of speciation at face value. You merely repeat "fruit flies are still fruit flies" with no peer reviewed studies and yet you've accepted that because it fits your prejudice.

It's not necessary for evolution to produce "new organs" to demonstrate speciation to have occurred. It is up to the creationist crowd to get busy and demonstrate how and why evolution stops at some "boundary" that they've made up out of whole cloth.

And you have the audacity to demand peer reviewed studied, when what you have is zip, zero, nada.

[Diamond]

By all means cite evidence of expression of a heavily methylated retroviral insertion.

I don't know about your qualification of "heavily methylated", but generally regarding trancriptionally active ERV's and protein expression in humans, as well as possible functionality, and interestingly, even insertion bias - Perpetually mobile footprints of ancient infections in human genome - Eugene D. Sverdlov

Cordially,

[Right Wing Professor]

The paper referenced does not claim LTRs are expressed. But regardless of whether retrotransposons sometimes have a functional role in humans, the occurrence of homologous retrotransposons in orthologous locations is strong evidence of common descent.

[Diamond]

The paper referenced does not claim LTRs are expressed.

Of course not, but it does suggest that LTR's are potentially able to cause significant changes in expression patterns of neighboring genes:

The number of described cases in which retroelement sequences confer useful traits to the host is growing. Retropositions can therefore be considered as a major pacemaker of the evolution that continues to change our genomes. In particular HERV [human endogenous retrovirus] elements could interact with human genome through (i) expression of retroviral genes, (ii) human genome loci rearrangement following the retroposition of the HERVs or (iii) the capacity of LTRs [long terminal repeats that are common to ERVs] to regulate nearby genes. A plethora of solitary LTRs comprises a variety of transcriptional regulatory elements, such as promoters, enhancers, hormone-responsive elements, and polyadenylation signals. Therefore the LTRs are potentially able to cause significant changes in expression patterns of neighboring genes.

The point I have made is that it is equally plausible that LTRs are of importance for some genomic purposes, but because we simply don't everything that they are doing in an organs, what their role was in the past, or how important their involvement is in genome functioning, the improbability of their presumed random coincidental insertion at identical locations of two different mammalian species is not necessarily smoking gun proof of common descent. After all, what would you say if the same ERV at the same location were found in two species that are not believed to have shared a recent common ancestor? Would you say that common descent had been falsified? I think not.

Cordially,

[Right Wing Professor]

The point I have made is that it is equally plausible that LTRs are of importance for some genomic purposes, but because we simply don't everything that they are doing in an organs, what their role was in the past, or how important their involvement is in genome functioning, the improbability of their presumed random coincidental insertion at identical locations of two different mammalian species is not necessarily smoking gun proof of common descent.

Retroviruses aren't simply retrotransposons. Most also have a coding region for an envelope protein. You also have to assume incorporation of the same retrovirus with the same envelope protein in the same place in independent events: and bear in mind retroviruses mutate far faster than their hosts. In fact, we do see evidence of incorporation of new insertions of some of the retroviruses by reinfection events (there was a paper in PNAS last year on this) and they don't go into the same site. There is even one element (K103) that most humans have, but that some sub-Saharan Africans have lost. That would tend to argue against functional significance.

Another problem is that the HERVs seem to have been incorporated a long time ago, and we've been slowly losing them. If they have a functional role or confer some advantange, then why were they only incorporated in a single burst, and why do they seem to be lost over time? Why are they apparently descended from only a small number of clades?

[js1138]

Oohhhhhh...

A real debate?

[Right Wing Professor]

A real debate?

Freaky, isn't it?

And neither Diamond nor I have called the other a moron yet.

[js1138]

I'm not sure I can stand it.

Unanswered questions...


The horror.

[William Tell]

Diamond said: "The whole proof of the common descent explanation lies in the vast improbability of mostly random viral insertions occurring in the same location in two different mammalian species because the DNA chain is too long for coincidence."

I am not confident that I understand what you are saying.

Let me try to restate it.

The evidence shows that artifacts, presumed to be caused by retroviruses, occur in the same genomic location of species which are presumed to share common ancestors. The presence of such artifacts is consistent with whether the artifact could have been present or absent in the presumed common ancestor.

I think that you are saying that there may be some enzymatic bias to "where" a retrovirus artifact occurs and thus the occurrences seen today are not descendant from a single infection event but instead just look like a single event.

If that is what you are saying and if that is what occurred, and given the very large commonality of genetic content for all primates, then wouldn't a great number of such artifacts have random frequencies? Wouldn't there be a majority of cases which would violate the presumed common ancestor appearance?

For example, humans share a majority of their genetic information with dogs, I believe. This would mean that at least half of the retrovirus artifacts which might appear in dogs could also appear in humans. This means that there would be a high frequency for artifacts found in humans and dogs, but not found in any other higher primates. Any enzymatic mechanisms would exist in both species with a frequency which matches the common genetic makeup.

If I understand the retrovirus evidence, it is the lack of artifacts in places where they could occur with a frequency dictated by common mechanisms but the presence of artifacts where they are consistent with common descent.