Evolution Question: Shared Ancestry / 'Family Tree' Evidence in the DNA

[lao tzu]

Well, what do you know. I'd never have believed we could have a meaningful post from the neocon voter. It's fundamentally wrong, of course, but it's still far more meaningful than I'd have given him credit for being able to create. There's nothing like making lowered expectations do your work for you.

Greetings, neocon,

but if HERVs have a useful function, you really don't have a slam-dunk here vis-a-vis shared ancestry.

The case for shared ancestry lies in the visibly hierarchical nature of the ERVs we find in the primate line. Here's a useful diagram to consider.

[attachment=1]

Source: TalkOrigins

The presence and absence of HERVs is responsible for the structure of this tree. If instead, say, there was an HERV shared between new world monkeys and humans, but not chimps, the tree structure would fall apart. This is not the case. There are no HERVs that break the tree.

You see, if there is a useful function, then the HERVs are located where they're supposed to be located, the same as other loci in the genome. And why wouldn't it be a similar location in the closest matching genome of the chimpanzee.

The real question is why they fall into a tree structure at all, not whether they are useful. It is the tree structure that leads us to the conclusion that there have been splits along the evolutionary corridors, and that is what makes the case for shared ancestry.

And it turns out HERVs so seem to have useful functions:

This is rather overstated, don't you think? Three slices of celery do not a stew make. And we can be fairly sure the celery is not thanking us for cutting it down in its prime for our needs.

At best, you make the case that some HERVs have been retasked. In fact, HERVs make up nearly 10 percent of our genome.

[attachment=2]

Source: Institute of Molecular Virology: Human Endogenous Retroviruses

Given the evidence that new functions for DNA are often co-opted through normal evolutionary processes and that HERVs are so common in our genome, it would be unusual to find no HERVs had found another job. But it's useful to keep in mind that these HERVs no longer perform their original function. If, for example, a portion of an ERV now performs an apathogenic function in a cat, we can be sure that was not its purpose before it was incorporated into the cat's germ line.

In fact, your examples are no more than what we expect, and simply do not make a case against shared ancestry.

As ever, Jesse

[rmwilliamsjr]

Given the evidence that new functions for DNA are often co-opted through normal evolutionary processes and that HERVs are so common in our genome,

google:
syncytin HERV-W placental attachment protein

[neocon_voter]

Well, what do you know. I'd never have believed we could have a meaningful post from the neocon voter. It's fundamentally wrong, of course, but it's still far more meaningful than I'd have given him credit for being able to create. There's nothing like making lowered expectations do your work for you.

Greetings, neocon,

but if HERVs have a useful function, you really don't have a slam-dunk here vis-a-vis shared ancestry.

The case for shared ancestry lies in the visibly hierarchical nature of the ERVs we find in the primate line. Here's a useful diagram to consider.

[attachment=1]

Source: TalkOrigins

The presence and absence of HERVs is responsible for the structure of this tree. If instead, say, there was an HERV shared between new world monkeys and humans, but not chimps, the tree structure would fall apart. This is not the case. There are no HERVs that break the tree.

You see, if there is a useful function, then the HERVs are located where they're supposed to be located, the same as other loci in the genome. And why wouldn't it be a similar location in the closest matching genome of the chimpanzee.

The real question is why they fall into a tree structure at all, not whether they are useful. It is the tree structure that leads us to the conclusion that there have been splits along the evolutionary corridors, and that is what makes the case for shared ancestry.

And it turns out HERVs so seem to have useful functions:

This is rather overstated, don't you think? Three slices of celery do not a stew make. And we can be fairly sure the celery is not thanking us for cutting it down in its prime for our needs.

At best, you make the case that some HERVs have been retasked. In fact, HERVs make up nearly 10 percent of our genome.

[attachment=2]

Source: Institute of Molecular Virology: Human Endogenous Retroviruses

Given the evidence that new functions for DNA are often co-opted through normal evolutionary processes and that HERVs are so common in our genome, it would be unusual to find no HERVs had found another job. But it's useful to keep in mind that these HERVs no longer perform their original function. If, for example, a portion of an ERV now performs an apathogenic function in a cat, we can be sure that was not its purpose before it was incorporated into the cat's germ line.

In fact, your examples are no more than what we expect, and simply do not make a case against shared ancestry.

As ever, Jesse

Hello, Jesse.

As I stated in POST 15, all was going to do was remove the slam-dunk status. I don't believe I ever implied that I had a slam-dunk refuting the case for shared ancestry. Sure most of these HERVs no longer perform a function, but all I really needed was just a single example to demonstrate a possibility of useful function. And even you have just implied that HERVs may have had a past function when you say:

quote = taoist
But it's useful to keep in mind that these HERVs no longer perform their original function.

The talkorigins tree does not refute the possiblity that HERVs were purposely located where they are located, since I noted that of course the location would be similar in a similar genome. Your 'real' question why they fit into a tree structure at all doesn't prove shared ancestry, anymore than a creationist claim that it proves a common design utilizing a basic plan based on DNA. One could create a similar tree with automobiles or appliances which we know aren't biologically related.

There is also the possibility that the ERVs were in place before the so called divergence of lines. The virologist who identified HIV, Robert C. Gallo, M.D., mentions (if I have interpreted him correctly) in VIRUS HUNTING Aids, Cancer, & The Human Retrovirus.
http://www.amazon.com/Virus-Hunting-...384049-6424953

VIRUS HUNTING: AIDS, Cancer, And the Human Retrovirus Robert Gallo MD page 97-98 ISBN 0465098150

Earlier Idiscussed how,like any bona fide virus, retroviruses can be transmitted as extracellular particles, sometimes also within infected cells, as may occur when there is blood contamination from one person to another. I contrasted these exogenous viruses to those endogenous viruses that are transmitted genetically in the germ cells (sperm and egg) in the form of DNA proviruses. I have noted that endogenous proviruses are ubiquitous: part or all of a provirus complement has been present in every vertebrate species where we have looked for them. It appears now that the LTR components of the proviruses are related to a large class of genetic elements that can change from one position to another in normal cell DNA. Those elements are called retrotransposons. They were first identified in lower forms of life such as yeast and are reminiscent of transposons -- genetic elements that change position -- which were first discovered in experiments with corn. Barbara McClintock received the Nobel Prize for this work.

These moving bits of DNA can have an important biological function, influencing the behavior of this or that gene of a cell, depending on their location at a given period. Perhaps retroviruses evolved from retrotransposons, becoming more complex. A more appealing possibility may be that retroviruses evolved with living forms almost from the start and, after becoming endogenous proviruses, often degenerated in time to become imcomplete proviruses and retrotransposons. Conversely, an endogenous retrovirus with full coding capacity to produce a virus may do so with the likelihood of eventually yielding variants that become infectious for the same animal species, or even escaping into a new species, now as an exogenous retrovirus. As I discussed earlier, this may lead to disease, particularly when the recipiant species has not previously experienced an infection with this kind of retrovirus. I wonder whether there is a cyclical process in its evolution: a sequence of exogenous virus --> endogenous virus --> defective endogenous virus --> retrotransposons, followed by the reemergence of a fully formed endogenous virus from retrotransposon and eventually back again to the infectious viruses.

© source where applicable

(emphasis mine, also forgive the over-citing but I want to make sure there is no implication of taking the author out-of-context)

Neocon_Voter

[chickenman]

in addition to ERVs, there are also processed and inactivated pseudogenes