Hi Ron
This is a good question. We know retroviruses can remotely alter a genome. There may be a purpose for this which is not yet discovered.
What appears though is that sequences that have been labeled ERV’s may have a definitive purpose in protecting the germ line.
We seem to be glossing over the evidence that different primates don’t share the same gene set.
You can just keep saying that no matter what. You could keep saying that after four thousand years of failure to discover a function.
Not only do you have no evidence that all ERVs are functional(much less that those few that are need to be fully intact ERV genomes to accomplish those functions), you’re also doing extremely poor philosophy of science here.
Effect =/= purpose. The “outside” has the effect of making the soles of my shoes dirty. That doesn’t mean that is it’s purpose.
Drool manifesting as text.
Post of the week!
No, they cannot. They must be present.
I guess we can add “remotely” to the long list of words you use but don’t understand.
No, we just don’t see how that’s relevant to anything. Please explain, if you’re capable of such a thing.
It’s not relevant if you have given up on the hypothesis that all primates share a common ancestor.
Especially given the fact the majority of ERV’s are solo LTR’s without any of the ORF’s needed for interference with incoming retroviruses.
What does that even mean?
Yet another example of your dogmatic position.
Why? Because you say so? Where is the evidence? Why does this discount their viral origin?
Exactly as we would expect from evolution with gene gain and gene loss.
It’s not relevant in any case. But I see that you indeed are not capable of explaining. This comes as no surprise, unfortunately.
You are shifting the burden and not addressed the issue. How do you support the single ancestor hypothesis for primates?
The null hypothesis is separate creation and that’s what the data currently supports until a mechanism that clearly explains the arrival of new genes is successfully demonstrated.
The pattern and sequence divergence of orthologous ERV’s, as one example.
False. The null hypothesis is not common ancestry. Nowhere in science is supernatural magic the null hypothesis.
Nested hierarchy. Duh.
I could go on.
You have no clue what “null hypothesis” means or how statistical testing works. And I see you make no attempt to explain yourself. You have also been shown at least two mechanisms that explain the origin of new genes: gene duplication and recruitment of non-coding sequences.
Ah, yes. As I pointed out some time ago:
Tell me, how soon are you going to recycle your other stock oft-debunked objections? It seems to me it’s been an unusually long time since you responded to a debunking about gene gains and losses by saying, “well, that doesn’t explain why there are any genes in the firrrrrrst place.” It’s important, you know, to keep your stale pseudo-objections on a reasonable schedule.
The two main obstacles for the claim of gene gain to overcome is the sequence problem and the waiting time problem.
Gene duplication and recruitment of no-coding genes does not address either of these issues unless there is a deterministic mechanism that does the recruiting and directs the change.
You have ignored all requests to explain what the “sequence problem” is. The waiting time problem is just a form of the Texas sharpshooter. But of course these two bogus problems do not even relate to common descent vs. creation, as they could be dealt with (if they actually needed to be dealt with) by appeal to guided evolution.
Why isn’t random mutation sufficient? (And note again that this is just a distraction from the issue of common descent vs. separate creation.)
Both non-problems. Do you have any substantive reasons to think that new genes cannot form?
Hi Andrew
Can you explain why you do not think these are problems?
@colewd, no matter how many times you deny it, the Southern corn leaf blight epidemic is an historical fact. You cannot make it go away.
@colewd, you really must think farmers are dumb.
Is this your paper showing exon recombination in plants?
