But if X occurs, then Y must necessarily occur unless there’s some barrier preventing infection of germ cells or preventing fixation of those mutations. Since there is no such barrier in either case, X is in fact evidence of Y. Consider your scenario, that retrovirus-looking sequences were separately created in the same spots in different species. What evidence could there possibly be for such a thing? What reason could there possibly be for such a thing? If it looks like a duck and quacks like a duck, why would you imagine that it’s a giraffe in disguise?
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As Phil Senter said, “if something looks like a duck, walks like a duck, and quacks like a duck, but religious dogma says it is a gorilla, then it is a gorilla.” This is an example of that ‘gorilla mindset.’
The large quantity of potentially rare events observed in the various populations.
If it looks designed therefor it is designed is ok?
Sounds like you should quantify that.
No, “looks designed” is too vague a claim to be examined. But we actually have a clear image of what retroviral insertions look like.
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So, by that standard, if we directly observed the Christian god creating a bunch of new “kinds” by intelligently designing them, you would not conclude that the “kinds” that already exist were descended from life forms he also created with intelligent design. Correct?
I don’t believe you answered the question that was implied in one of John’s responses above.
Your rcomment above would entail that it is impossible for retroviral insertions to become fixed in a population. This would make them very different from any other mutation. How do you justify your belief that ERV insertions are prevented from becoming fixed? What process would prevent this?
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What you don’t know is the various functions of sequences that look like retroviruses. The article above (and supporting paper) that Fazale of RTB wrote appears to have found an important one.
Ok. Now we recognize clearly the objection to ID is subjective.
False. It is not a fallacy to conclude that a fingerprint at a crime scene was put there by a finger. The same applies to ERV’s and retroviruses.
We already have tons of models demonstrating mutations moving to fixation. Do you reject pretty much all of population genetics?
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We don’t need to know their current function in a host genome in order to know their origin.
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So on the one hand, you think the fact that we have directly observed the endogenization of retroviruses does not mean that what look identical to endogenized retroviruses in our genome actually are endogenized retroviruses.
On the other hand, you believe the fact that a minute portion of these ERV’s have been found to have a function means that they all probably have functions.
I’m just pointing out the utter intellectual vacancy and incoherence of your position. No need to respond.
ID Creationists don’t do pop gen. Few of them even know what it is.
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And you assume that because one ERV has a function, all of them do? Why? And why do they look exactly like retroviruses?
“We”? Do you have an intestinal parasite?
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I do not assume this but the paper that Fazale based his article on shows that the transposons sequences in koala bears can recombine with RV’s and neutralize them. As Behe might claim a purposeful arrangement of transposable elements.
Have you read that paper to see what it actually says?
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I have read the abstract and skimmed the paper.
Retroviral elements that emerged by endogenization(degradation and inactivation) of retroviruses are now, following their endogenization, “purposefully arranged” in a way where recombination between the old degraded ones and the new invasions, makes subsequent endogenization of the new retroviral insertions even more likely than it already was. Because this destroys the function of the new one.
You know retroviruses don’t have to be functional for recombination between homologous sequences to inactivate new retroviral insertions, right?
It is the fact that the old insertions, the degraded ones already present, are nonfunctional but still get transcribed, that makes their recombination with transcripts from new infections inactivate the new ones so they too become nonfunctional.
It is their having sequence-similarity that allows homologous recombination, and it is the old and degraded one’s lack of function that inactivates the new ones when they are combined with the old ones.
Once the RNA gets reverse transcribed back into DNA, you get another nonfunctional ERV insertion.
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Here is said abstract:
Endogenous retroviruses (ERVs) are proviral sequences that result from colonization of the host germ line by exogenous retroviruses. The majority of ERVs represent defective retroviral copies. However, for most ERVs, endogenization occurred millions of years ago, obscuring the stages by which ERVs become defective and the changes in both virus and host important to the process. The koala retrovirus, KoRV, only recently began invading the germ line of the koala (Phascolarctos cinereus ), permitting analysis of retroviral endogenization on a prospective basis. Here, we report that recombination with host genomic elements disrupts retroviruses during the earliest stages of germ-line invasion. One type of recombinant, designated recKoRV1, was formed by recombination of KoRV with an older degraded retroelement. Many genomic copies of recKoRV1 were detected across koalas. The prevalence of recKoRV1 was higher in northern than in southern Australian koalas, as is the case for KoRV, with differences in recKoRV1 prevalence, but not KoRV prevalence, between inland and coastal New South Wales. At least 15 additional different recombination events between KoRV and the older endogenous retroelement generated distinct recKoRVs with different geographic distributions. All of the identified recombinant viruses appear to have arisen independently and have highly disrupted ORFs, which suggests that recombination with existing degraded endogenous retroelements may be a means by which replication-competent ERVs that enter the germ line are degraded.
Bill interprets this as evidence that all ERV’s are functional genes created by a god.
The mind boggles.
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Why not just purposefully, you know, not invent the RV’s? Then you would not need purposeful ERV’s sequences to counter the RV’s you made.
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Yeah. Bill can’t fathom a 2-sentence post written by someone going out of their way to make it comprehensible to him. Why would he be able to understand an entire paper written for other professionals in the field?
He probably didn’t even read it all. He probably just read the title, and then skimmed the abstract only.
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Now that’s really interesting. It’s such a shame that ID proponents will just continue to use this as rhetoric, even though it doesn’t support their position, and never stop to consider how cool it is that ancient infections can help prevent modern infections due to recombination.
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I fail to see how even that would give someone the impression that ERV’s are all functional. “Degraded” does not generally translate to “functional” in any context. Fuz Rana also wrote some stuff that he seems to have read so that is probably further addling his brain. Addled brains is what the creationists want to produce.
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It wouldn’t. He got that idea from some “reasons to believe” apologist who made it up as a rationalization. Apparently it was Fazale Rana who thinks these degraded ERV insertions are “functional” because their nonfunction breaks novel ERV insertions when they’re recombined.
It functions by being nonfunctional. Brilliant!
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