Not always huh? So how often? Out of all introns excised from pre-mRNA, how often is one circularized, retained, and shown to have a selected-effect function? Give me a percentage and a reference.
So what percentage of introns did you predict would be circularized, retained, and demonstrated to have a selected-effect function, in 2010?
I wish I had time to read these books. In the meantime, it seems to me that the first issue that would need to be solve in order to decide whether the origin of species is really understood would be to have a clear notion of what species are, which doesn’t seem to be necessarily the case.
The first mistake is expecting biology to fit into neat little human constructed boxes. There is no reason to expect that there should be hard and easily defined borders between species, especially with a continuous process like evolution. It’s like trying to divide the entire human population into young and old. Everyone can see that there are old people and young people, but the line between them is always going to be arbitrary.
You could stop spreading creationistic misinformation on the internet, then you’d have a lot more time on your hands.
The most common definition is two groups of animals are considered different species if they no longer exchange genetic material between their respective gene pools. Not that they can’t interbreed, it’s that they don’t. Since the real world is an analog place there are always going to be gray areas along the boundaries with no clear line of demarcation.
The reason speciation is important when discussing GE is the process of speciation - new species arising from older species - has been going on for a few billion years. It doesn’t matter if older species have gone extinct (which 99% of them have) as long as they split and produced new species. Every creature alive today can trace its roots back those billions of years. At every step, every generation, every species over that time frame had a viable genome which gave rise to a later viable genome.
Since the process of speciation doesn’t magically “reset” a genome into some undefined “perfect” condition that means no genetic entropy causing life to go extinct.
Do you understand what I’m explaining to you? Sanford’s whole GE idea is based on the YEC premise all extant species were specially created with “perfect” genomes only 6000 years ago. That idea was falsified 160 years ago. Sanford may be a nice guy but his GE is a non-scientific crank idea put forward only to support his YEC views.
Here is a possible scenario:
Just as there are stem cells in ontology that can give rise to a variety of more specialized cells, there may have been in philogeny some “stem” organisms resistant to genetic entropy that would have given rise to a variety of more specialized organisms, aka the species.
That makes absolutely zero sense. ALL extant species come from an unbroken line of descent going back to the first self replicating life forms. That means they ALL must be “resistant to genetic entropy”.
Sorry but Sanford’s GE is deader than the proverbial doornail.
Alrighty, although I think I provided many data points so far as to the change in sentiments for introns, I can provide more. This will also lead to the problem of Slight Deleterious Mutations (SDM) that are important to the genetic entropy hypothesis.
Regarding the paper in intron function in yeast under a starvation stress response, this is important in that it might have been naively assumed that the introns served little to no role if the experiment had not been conducted under stress conditions.
The 2019 paper I cited earlier in this thread was:
Introns are mediators of cell response to starvation | Nature
Introns are ubiquitous features of all eukaryotic cells. Introns need to be removed from nascent messenger RNA through the process of splicing to produce functional proteins. Here we show that the physical presence of introns in the genome promotes cell survival under starvation conditions. A systematic deletion set of all known introns in budding yeast genes indicates that, in most cases, cells with an intron deletion are impaired when nutrients are depleted. This effect of introns on growth is not linked to the expression of the host gene, and was reproduced even when translation of the host mRNA was blocked. Transcriptomic and genetic analyses indicate that introns promote resistance to starvation by enhancing the repression of ribosomal protein genes that are downstream of the nutrient-sensing TORC1 and PKA pathways. Our results reveal functions of introns that may help to explain their evolutionary preservation in genes, and uncover regulatory mechanisms of cell adaptations to starvation.
Since the advantage of introns can be especially evident under stress conditions, it stands to reason selection to preserve them under non-stress conditions is relaxed, hence it would be easier for slightly deleterious mutations to slowly compromise a population.
In the context of humans, a comparable situation exists for slightly deleterious mutations in as much as technology and medicine are relaxing selection against things like juvenille diabetes, and hence it is harder for the population on the whole to get rid of function compromising mutations.
To the extent introns in humans possess important stress response mechanisms, mutations in these regions would be under relaxed selection and thus could accumulate. But even beyond that, the Bonker’s formula and the Muller limit presented earlier makes some of the issue of selection strength somewhat moot in a situation where the mutation rate is high.
Good! The conversation has drifted a bit and it would be nice to get back on track.
Are you trying to be funny? If so, well done!
You have not. You have provided references that suggest ways in which putatively functional introns could be functioning.
No, it won’t “lead to” that in any way. You are just making that up out of nowhere.
What introns specifically? Who is supposed to have assumed those(or all) introns are nonfunctional? In what species?
The fact that you can delete a huge number of introns and then find that among all those deletions, some cause a physiological response in some particular species doesn’t mean all, nor even the majority of all introns in all species are functional. You’re going to have to do more work to find out which particular introns are producing what effect, and then you’ll need to find out how conserved those particular introns are to see if they are among those that would have been predicted to be nonfunctional. None of which you have done.
There are considerable differences in the intron density in similar genes among different eukaryote species, among other reasons because selection have been much more effective in single-celled organisms with large population size, such as yeast. As a consequence, they have way fewer introns/gene compared to large multicellular eukaryotes like plants and animals. As a consequence a larger fraction of their introns could constitute those having been retained because they were functional.
As usual you’re making vague and grandiose extrapolations from limited data, and assigning absurd and absolutist strawmen positions to people that they don’t hold.
Did you actually read that paper you cited, or did you just find something to throw some squid ink while you make your getaway? The people who study speciation (at least in those books) are using the biological species concept, which means that speciation involves the evolution of reproductive isolation between two populations. The difficulty you’re trying to create does not exist.
There is no evidence for such a thing, and there is no mechanism by which such a thing could happen. This is unjustified special pleading.
Sternberg laid out succinctly on June 3, 2010 what I have said in this discussion. However at the time, some of the claims were somewhat tentative relative to what we know 10 years later.
non-translated microRNAs regulate the developmental expression of messenger RNAs, and small nucleolar RNAs are essential for the processing of ribosomal RNAs (which in turn are essential for protein production). The human genome contains 1,664 known genes for the former and 717 known genes for the latter, and the majority of these genes occur in introns .
Then there are the regulatory codes associated with such RNA genes, which also occur in introns. And RNAs that emanate from introns but that are not part of messenger RNAs; 78,147 of them are known to exist in humans. Even if only ten percent of the latter RNAs play some role in cellular organization, we have far more than “a handful” of functional introns in this category alone.
And there’s still more. RNA is essential for chromatin organization in the nucleus. When chromatin-associated RNA is degraded by experimental means, the geometry of chromosomes and nuclear metabolism is adversely affected. Yet a recent study of this class of RNAs in human cells revealed that over half of the transcripts (52%) are derived from… introns!
I could go on. Various DNA control modules have been mapped to introns, including alternative promoters, enhancers, silencers, and nuclear matrix attachment sites–some of which influence genes that are located over a million basepairs away on the chromosome. But sorting through all the studies that have been published on this subject would be a big job.
The change since 2010 is that Sternberg’s claims just needed more experimental confirmation and broader acceptance and awareness.
There is no one description of what an intron does any more than trying to say what a protein does since there are so many possibilities. It seems we’re realizing some of the functions of introns are becoming somewhat gene specific.
Sternberg notes:
non-translated microRNAs regulate the developmental expression of messenger RNAs
and half of these microRNAs (miRNAs) come from introns. Micro-RNAs are small, about 22nts. But for them to function require incredible coordination in the genome since a single miRNA may regulate mutliple genes through interacation the messenger-RNAs (mRNAs). This means the multiple genes regulated by an miRNA must have the proper target recognition sequence put in them. How could so much coordination across mutliple genes evolve to be regulated by the miRNA from an intron?
To illustrate the regulatory complexity of a miRNA network consider the diagram below:
To get an idea of the levels of interaction consider how this diagram
accounts for Intronic RNAs and histone markings in a gene regulatory network!
from: >https://www.sciencedirect.com/science/article/pii/S2211124715014552
And THAT is just a fraction of the roles of introns! The complexity boggles the mind.
Does anyone know why Sal is doing all this tap-dancing and hand-waving? Sanford’s GE idea has already been conclusively disproven by the fact we have life (and the associated genomes) being on the planet for billions of years while NOT going extinct from “genetic entropy”.
stcordovaSalvador Cordova Young Earth Creationist?
Yep, with a literal Noah’s Flood and everything. Although sometimes he claims to be a “Young Life Creationist” which makes even less sense.
The reason I’m going through all these details of introns, etc. is that Sanford’s genetic entropy thesis is supported by the spirit of this statement by Graur:
If ENCODE is right, evolution is wrong
But we can just as well say
If the percentage of human genome function is high, evolution is wrong
This can be argued in multiple ways, but the simplest is the Bonker’s formula
\large {NumberKidsPerFemale} = 2 e^U
where U is the number of mutations.
It just so happens that for every 1% of the genome that can be reasonably argued is function, that makes the problem about 5.4 times harder for evolution because each human female needs to be making 5.4 times as many kids. At one end of the extreme, even Graur said, each female would need on the order of 10^35 kids. And commented, “this is clearly BONKERS!”
Introns account for a lot of non-coding DNA. Unfortunately, the introns are not a disjoint group from other ncDNAs like ERVs and Alus since these can be inside introns…
That said, ERV were also once said to be functionless parasitic junk. It turns out they are often targets of the zinc finger proteins like the CTCF zinc finger protein. And this plays an important role in gene regulation. Here is one example:
Endogenous Retroviruses Function as Gene Expression Regulatory Elements During Mammalian Pre-implantation Embryo Development - PMC
Endogenous Retroviruses Function as Gene Expression Regulatory Elements During Mammalian Pre-implantation Embryo Development…ERVs provide binding sites for a chromatin organizer, and then participate in the formation of a high-order chromatin structure.
There are other examples of zinc finger proteins like KRAB-KZNF. The DNA-binding site in the diagram below is often an ERV or some other non-coding element!
But what is most amazing is how the ERVs or other CTCF binding sites have to be gramatically or geometrically oriented to enable creation of regulatory loops.
See this 3-minute video, and remember each time you see the “CTCF motif”, that is often an ERV or some other “junkDNA” that makes the system possible! Note the “junkDNA” has to be pointed in the direction of the arrows to make this system work.
This also suggests the ERVs (or other “junkDNA”) aren’t randomly positioned unless it was an accidental mutational deviation from a healthy state. Given these kinds of DNAs can jump around, such transposition mutations to the DNA may create defects that will disrupt the normal looping of DNA resulting in genetic degeneration over time.
Heh. Sal still thinks quote-mined quotes and pretty colored diagrams magically invalidate 160+ years of consilient scientific evidence falsifying Sanford’s GE brain fart. 
Here’s a hint Sal. If you’re trying to massage your steaming pile above into another “lesson” for your Creation class you’re wasting your time. Like everything else you try to twist it’s a 100% loser.
Look at those pretty figures. So many arrows, colors, abbreviations. So technical. So science.
Yes, I do. But this is Peaceful Science, so I won’t say more. 
