Given that I presented a case in which removal of the endogenous retrovirus had a clear effect by restoring the wild-type phenotype, your statement makes no sense at all.
Of course, that’s an exception. You’re trying to pretend that the scientists here are asserting something global when not a single one has done so.
How do you know that ERVs originate from retroviruses ? Can’t we imagine that ERVs were placed in the genome by the creator to occupy a function where resemblance to retroviruses is important ?
Ok. But what are these multiple independent lines of evidence then?
This is the equivalent of saying that dinosaurs never existed. Instead, what we think are dinosaur fossils are actually structures that God included as part of the earth because they serve an important function.
If we can formulate testable hypotheses as to how and why a creator did a such thing, then sure. We would need to be able to distinguish a retroviral insertion versus something that was created with the appearance of a retroviral insertion.
Any thoughts on how we can accomplish that?
Otherwise you’re just invoking a variation of the Omphalos hypothesis, which adds nothing useful to the equation.
That’s like saying because someone once restored a car from the junkyard to a functional state (or grabbed some spare part from it), then maybe all (or the majority of) the cars at the junkyard were placed there to serve some important function where looking like a car that was discarded as junk is important.
Meanwhile a much simpler explanation is that they’re just discarded junk cars.
If this isn’t just rhetorical then I am surprised you need to ask considering how many times the concept has been discussed around here. Two excellent sources:
Alternatively you can watch this nice introduction to the concept:
A quick list off the top of my head of the different lines of evidence for mostly junk genomes in most large multicellular eukaryotes:
Interspecies and intraspecies variations in genome size (The Onion Test)
Lack of both sequence (and length, see genome size) conservation for the majority of the genome
Most of the genome size (and intra and interspecies variations in it) comes from DNA that has the capacity to selfishly copy itself (transposons and ERVs)
Most of these are decaying copies at various stages of mutational decay
Evidence from mutational load/population genetics
Large numbers of inactivated pseudogenes
Large amounts of repetitive DNA (also prone to expand or contract in size over generations due to, among other mechanisms, unequal crossover, strand slippage, and other causes of duplications and deletions)
I think that’s about the gist of it. Maybe others can add something I’ve forgotten.
Obviously every single piece can be offered some alternative ad-hoc rationalization for why it needs to be that way to serve some undiscovered/yet-to-be-elucidated function, but there’s no single competing hypothesis that explains all the same facts like the junk DNA hypothesis does.
Many reasons. They’re mostly not fixed, i.e. their presence varies among individuals so they can’t be essential. The active ones actually do make new insertions. Their sequences are not conserved. The insertions, active or inactive, shared among species follow a nested hierarchy. None of these facts are expected under your hypothesis.
Let us also add @Rumraket’s list of evidence favoring junk DNA, of which ERVs are mostly a part.
Also, I concur with @Mercer’s prediction that you will ignore all of this.
Thanks to you and @Rumraket for the evidence you provide in support of your view. Don’t think that’s the end of the matter, though, for it seems clear that ever since Barbara McClintock’s pioneering work, more and more non ID scientists are suspecting that far from being junk, mobile genetic elements play important roles not only in the biological operations within individuals but also in evolution. Maybe my favorite one is James Shapiro and his natural engineering hypothesis.
Those aren’t mutually exclusive. Most are junk, a few become functional, and this can be important in evolution. But James Shapiro is a well-known crackpot, even though he’s a real biologist. But have you abandoned YEC in favor of evolution guided by the organisms themselves?
Ignaz Semmelweis, Alfred Wegener, Barry Marshall, Robin Warren and others in the history of science were also ridiculed or dismissed as crackpots but eventually were proven right.
I’ve said countless times in this forum that I am not a YEC! I am an ID proponent, more of the Behe type.
Please explain why you believe McClintock’s work refutes every one of the multiple lines of evidence that @Rumraket provided. Or, for that matter, refutes even a single one.
And a few examples here and there have been found, though the 7 or more lines of evidence I referred to above still supports the vast majority as being junk.
None of this evidence goes away, it doesn’t get rebutted or even responded to, by name-dropping scientists suggesting the possibility that more mobile genetic elements could have functions.
…for certain values of “right”. But sure. Is that, however, the way to bet? If you looked at the entire population of crackpots at any one time or through all history, what proportion would eventually be vindicated? In the words of Carl Sagan, " They laughed at Columbus, they laughed at Fulton, they laughed at the Wright brothers. But they also laughed at Bozo the Clown.”
Do you not frequently argue against common descent, or am I confusing you with someone else? Perhaps you could present your position on evolution briefly, and not just by dropping a name or two, but by explaining what you think has happened in the history of life, especially what God might have done and when. That might clear up my confusion.
As I understand Behe, he agrees that all life is related by descent, but that God is necessary to explain certain inferred mutations or combinations thereof. You?
@Giltil: Incidentally, at various times in the past you have posted to cast doubt on radiometric dating, phylogenetic analyses, and other things that Behe would disagree with you on.