I had to look up "porkies" in a
dictionary. The only definition that even remotely makes sense in that sentence is "lie".
That's correct... I have produced research that strongly suggests introns located in similar loci does not necessarily suggest common descent....and this is just one more example of how your algorithms are erraneous.
ALL THE EVIDENCE YOU PUT FORWARD FOR ERVS IS PRESUMPTIVE FLAWED ALGORITHMIC NONSENSE BACKED BY OTHER RESEARCH, BASED ON THE SAME ASSUMPTIONS AND OFFERED AS EVIDENCE. IT ISN'T.
Please tell me why what you quoted there is a lie? I thought it was simple logic.
You and Loudmouth said ERV's have nothing to do with introns...A LIE.
Because I thought LM was doing a splendid job of it.
He wasn't!
Care to quote the particular claim of evidence you are referring to?
I did. I posted research that suggests LTR/ervs are found in introns and research that suggests ervs are less likely to be found in introns. Are you silly enough to place your credibility on one of them beoing correct. It is more likely that both are nonsense and neither are correct...as erv's are functional, where they are meant to be to provide gthe function they were designed for,
No one said there were no ERVs in introns. (Please quote to correct me if I missed something...)
You said erv's have nothing to do with introns...a lie.
By the way, what is your argument? Earlier on, it seemed to be that ERVs are functional. The passage you quoted here implies that most ERVs are not only not useful, they can be
harmful.
I can pull research to support whatever I want. So can you. That is the beauty of your science. Here is some that supports both beneficial and harfull effects of ervs.
"This article has provided an overview of a complex topic that may have ramifications in host protection, cancer, and autoimmunity. Ultimately, are HERVs friends or foes? In conferring a biological advantage, HERVs (and solitary LTRs) may indeed be beneficial. Their role in immunological homeostasis and perhaps protection against exogenous retroviruses is intriguing. Alternatively, HERV insertion mutation, molecular mimicry, superantigen motifs, and recombination with other viruses could be responsible for the development and pathology of disease. An additional aspect is whether the presence of HERV peptides during ontogeny culminates with a hole in the immune repertoire. As a result, peptides with similarity to HIV-CTL sequences could be more dangerous to a given individual."
Demystified . . . Human endogenous retroviruses
I'm glad you reckon evolution is smart enough to know what exactly a beneficial mutation is because your researchers surely don't.
Either I got lost in your reasoning, or you just shot yourself in the foot.
I'd say it was a head shot to your head, but you still can't see it!
Also, did anyone here claim that
introns served no function?
Neither did I. You are so confused I do not think you have any idea where you are going.
No one said they weren't found in introns. What (I think) Loudmouth was trying to tell you is that introns are functional =/=> ERVs are functional.
The point is the research demonstrates that the very reason you lot suggest identical loci is suggestive of common descent is now challenged. You can go around in circles all you want...and this is just one point in alist of nonsensical misrepresentatons re ervs.
"In addition, we believe our work facilitates a more accurate estimate of intron gain rates, and directly challenges the assumption that parallel intron gains are rare in many prior analyses."
"Remarkably, we have found many cases of parallel intron gains at essentially the same sites in independent genotypes," Lynch said. "This strongly argues against the common assumption that when two species share introns at the same site, it is always due to inheritance from a common ancestor."
Introns -- nonsense DNA -- may be more important to evolution of genomes than thought
No, we call that "forming hypotheses". Your attempts at understanding what's going on are also quite hilarious.
Loudmouths assertion and yours that ervs have nothing to do with introns is funnier coming from folk that pretend to know what they are talking about.
What's the problem with the algorithms used, then?
They are based on assumption. Ignoring the posts I put up and constantly requesting support for each of my points over and over is just showing how little of you know of this science you defend. You didn't think evolutionary science was real science, did you?
Although molecular systematists may use the terminology of
cladism, claiming that the reconstruction of phylogenetic relationships
is based on shared derived states (synapomorphies),
the latter is not the case. Rather, molecular systematics is
(largely) based on the assumption, first clearly articulated by
Zuckerkandl and Pauling (1962), that degree of overall similarity
reflects degree of relatedness. This assumption derives
from interpreting molecular similarity (or dissimilarity) between
taxa in the context of a Darwinian model of continual
and gradual change. Review of the history of molecular systematics
and its claims in the context of molecular biology
reveals that there is no basis for the “molecular assumption.”
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In what way does the stuff you showed about their distribution contradict that idea?
Let's see.
They are preferentially located in intergenic regions, and avoid introns.
This is pointless. You'll go on for years about nothing thaat has has anything to do with the point I am making. See below..now woffling on about the reasearch which was quoted to demonstrate the erraneous nature of your algorithms. You appear to be confusing yourself!
When they
are in introns, they are more often oriented opposite to the gene, even though they seem to insert without a preference.
Bla bla...see you at the end of your post....
That just looks like retroviruses that insert in introns, and especially those that insert in introns in the wrong direction, are selected against.
Being selected against is truly the hallmark of useful DNA.
If you care, I can mock up an explanation for both of those observations right here. Why are ERVs purged from introns? Because being in an intron means the virus is transcribed every time the cell needs the host gene. Shortly after insertion, the ERV will still be active. Transcribing it is basically setting it loose on the genome. Do it enough times, and you'll get an insertion somewhere really important.
I do not need to mock anything. Your researchers do a great job of mocking and refuting each other. Who am I to interfere?
Why are
sense-oriented ERVs especially purged from introns? Because the above is only a risk if the virus shares the orientation of the host gene. A gene is only transcribed from one strand of DNA. If the virus is on the other strand, transcribing the gene won't touch it.
See, here's my hypothesis based on the assumption that ERVs are useless at best, and active ERVs are harmful.
Oh wow.....you have less idea than I thought really! Read above, erv's can be both advantageous and deleterious. Really, the truth be known, your researchers have no clue....You have made a false assumption then...Why am I not surprised. As I said, with what is observed rather than speculated, your researchers have no idea what is advantageous or not....
Shall we see
your interpretation of the same data, based on the assumption that ERVs are useful?
Oh boy!!!!
Better learn to live with that. If memory serves, pieces of virus occupy about four times as much of your genome as your own proteins. We are, shall we say, heavily parasitised...
How about you go do BIO101, again and stop wasting my time.
It is called "understanding what the hell is going on", I believe.
You and your researchers obviously do not know what is going on yet you and all still faithfully believe!