Art Hunt, June 14, 2010:
As far as the functional vs. non-functional business, there is one key fact that IDists ignore in all of this. I refer, of course, to the fact that intronic RNA is made and then thrown away. We don’t call it “junk” because we don’t know if it does anything, we call it so because it is discarded.
–Arthur Hunt
Sternberg Plasters Matheson, Comment #357009
Ah yes, so nice to see the data finally siding with my suspicions 10 years ago and against what Art postulated.
In the paper below, the authors provide evidences that changes in codon usage within a RNA virus reduced its robustness and attenuated the virus in an animal model of infection.
https://www.cell.com/cell-host-microbe/pdf/S1931-3128(12)00353-8.pdf
This one also, where, regarding selection at synonymous sites, the authors say « We estimate that this type of selection contributes approximately 18% of the overall mutational fitness effects in ssRNA viruses under our assay conditions and that random synonymous substitutions have a 5% chance of being lethal to the virus »
It’s not always thrown away:
Exon-intron circular RNAs regulate transcription in the nucleus - PubMed
A vast number of circular RNAs (circRNAs) have been identified, and some have been shown to function as microRNA sponges in animal cells. Here, we report a class of circRNAs associated with RNA polymerase II in human cells. In these circRNAs, exons are circularized with introns ‘retained’ between exons; we term them exon-intron circRNAs or EIciRNAs. EIciRNAs predominantly localize in the nucleus, interact with U1 snRNP and promote transcription of their parental genes. Our findings reveal a new role for circRNAs in regulating gene expression in the nucleus, in which EIciRNAs enhance the expression of their parental genes in cis, and highlight a regulatory strategy for transcriptional control via specific RNA-RNA interaction between U1 snRNA and EIciRNAs.
My view in 2010 is vindicated yet again.
That is not my take away at all. The paper assert that RNA viruses come under more selective pressure in response to synonymous mutation. Robustness is not mentioned in terms of consequence or viral functionality, and attenuation is not mentioned at all. Also, these were bacteriophages, large animals were not infected.
From the paper, bold added:
Analysis of this mutant collection and of previous studies undertaken with a variety of single-stranded (ss) viruses demonstrates that selection at synonymous sites is stronger in RNA viruses than in DNA viruses. We estimate that this type of selection contributes approximately 18% of the overall mutational fitness effects in ssRNA viruses under our assay conditions and that random synonymous substitutions have a 5% chance of being lethal to the virus, whereas in ssDNA viruses, these figures drop to 1.4% and 0%, respectively. In contrast, the effects of nonsynonymous substitutions appear to be similar in ssRNA and ssDNA viruses.
…Selection acting on synonymous substitutions should be most relevant in viruses with highly compact genomes because their protein-coding sequences are often involved in gene regulation, cell trafficking, or virus encapsidation. Particularly, it has been shown that some of the secondary structures adopted by RNA virus genomes are under strong selective pressure because they regulate translation …, control replication initiation …, or are targeted by cellular RNases
…the overall mutational robustness of ssRNA and ssDNA viruses is similar, albeit slightly greater in the former.
So a given viral particle may be subject to a synonymous mutation. It is especially likely as a RNA virus that this be deleterious and subject to selective pressure and outperformed by the hoards of unmutated kinfolk viruses. That is exactly in accord with conventional statement of natural selection. There is no support in this paper for the idea that slightly deleterious mutations sneak in under the radar and accumulate until some final straw on the camel’s back results in catastrophe. Attenuation happens in epidemics, but for reasons unrelated to genetic entropy.
So, @stcordova, just how many introns end up in circular RNAs? What percent of all introns is this?
So, @stcordova, what percent of the genome of budding yeast coded for introns? What is the relevance of the paper you cite to mammalian molecular biology, and especially “genetic entropy”? Do you even understand how confused your arguments are becoming?
“Ten years ago, they said most swans were white. I bravely disagreed, and said that white swans did not exist, and that all swans are black. Then, when the finding of a black swan was reported, I was vindicated.”
That about it, Sal?
No one knows, but the point that was vindicated on my part was that it was pre-mature to insinuate it was all junk because it didn’t leave the nucleus. All that had to happen to prove your claim wrong was that SOME of the intron RNA transcripts had function.
I thought your pronouncement in 2010 was terribly presumptuous and premature, and I was right. I kept my eye out for some sort of RNA-based gene regulation, and my search didn’t dissappoint!
It’s the “throw crap at the wall and see what sticks” approach. Not like we haven’t seen Creationists do this before. 
Hi Gilbert,
Just an FYI – the reason I haven’t weighed in on the virus issues is that it is not the area Dr. Sanford assigned me to focus on with respect to Genetic Entropy. He wanted me to focus mostly on human and mammalian genomes.
Dr. Carter is the best resource on the issue of H1N1, not me.
Nevertheless, (and I think I can speak for Dr. Sanford), thank you for your interest and support for the further discussion and investigation of the Genetic Entropy hypothesis.
I hope you’re enjoying my side of the discussion on the human genome.
Well, between that and overturning geology and the physics of radiometric dating, I would grant that you have a pretty full agenda.
Not only is it lacking evidence to support it, but there seems to be a lot of evidence against it. Influenza A is an RNA virus that does not insert into the host genome. It has no reverse trascriptase, and it uses an RNA dependent RNA polymerase, which means there is no DNA intermediate. From what I have read about episomal latency, it requires a DNA genome or intermediate. Therefore, the only natural reservoir influenza A has is to continually infect a host population, be it humans or some other animal (e.g. chickens, pigs). Since the virus would be continually infecting and copying its genome this type of reservoir will not protect it against Genetic Entropy.
Since influenza A has to continually replicate and infect new hosts in order to survive, why hasn’t it disappeared or gone extinct?
It is also pre-mature to insinuate that DNA has function simply because it is transcribed.
You would be wrong if you can only find a tiny percentage of transcribed introns that function in gene regulation. The percentage of functional sequence in introns is important.
That was a generalization, and it still holds today. The vast, vast majority of RNA from introns doesn’t leave the nucleus and lacks evidence for function. If you are going to claim that the vast majority of the human genome has function you need to do more than find a tiny portion of introns that have function.
The possibility was explored through the comparison of genomes between species. The best candidates for functional DNA are those stretches that have evidence of sequence conservation. Those are what scientists are focusing on.
What you need to explain is how 90% of the human genome can have function while lacking evidence of sequence conservation.
I’m not claiming that, I pointing out reasons it’s premature to say it’s junk, and the last line of reasoning one should use is that “it’s junk because it disagrees with what evolutionary biologists think”.
Quote specifically where I stated that 100% of all intronic RNA/DNA is junk (especially because it doesn’t leave the nucleus). Be specific. If you cannot, a retraction and apology (not to me, but to the discussion board for lying about what I said) is in order.
You haven’t presented any of those reasons. We conclude that most of the human genome is junk because it doesn’t show any evidence of sequence conservation. Finding snippets of conserved non-coding DNA does nothing to change this conclusion.
This is what I quoted:
Art from 2010:
The issue was that you said intronically generated RNAs that left the nucleus "is made then thrown away and therefore “we call it so because it is discarded” which is an equivocation at best and faulty logic at worst.
I showed two papers that gave evidence that they aren’t junk just because they don’t leave the nucleus. In fact, they should stay in the nucleus to fulfill their regulatory purpose.
It would be in order if were lying, but I quoted you from 2010, and I criticized exactly why it was wrong. Just because intronically generated RNAs don’t leave the nucleus doesn’t mean they are junk, whereas you yourself said 10 years ago.
So you were apparently relating the supposed lack of function in introns based on their RNA transcripts remaining in the nucleus. Even a non-biologists like me at the time 2010 (before I got my MS equivalent in biology) could see that was an ill-advised, presumptuous, pre-mature claim.
When I studied at the NIH a professor of my micro-RNA class, when talking about RNAs in general said, “if it’s there, is gotta be doing something”. NOT that he’s necessarily right, but that certainly echoes a lot of sentiments in the medical research community. Whether he was right or not, it’s a lot better heuristic than blindly assuming, as you did in 2010 that it was junk because it didn’t leave the nucleus. You yourself related it to the question of the functional vs. non-functional business,
Or are you claiming now, that your assertion of intronic RNA staying in the nucleus had nothing to do with the functional vs. non-functional business ?
No, you haven’t done that.
Why? We’ve long since established that evolutionary biology provides a largely accurate account of life on this planet. You’re aren’t seriously suggesting that biologists should pretend that evolution isn’t true, are you?
That is an accurate generalization. It is no different than saying birds fly through the air, even though a handful of them don’t.
You did not show us a paper that gave evidence for 100% of intron sequence, or even a majority of it. You cited evidence that a tiny percentage of intron sequence has function which does nothing to change the conclusion that the vast majority of introns lack function.
Many Micro-RNAs are strongly conserved across species.
However, there is no reason to think that DNA has function because it is transcribed into a few copies of RNA in some cells. There is no reason to think that mechanisms of RNA trascription are so accurate that they would not transcribe junk DNA.