In the 1970s, when scientists compared the sequences of DNA in genes with the sequences of RNA encoded by those genes, they made a puzzling discovery: the DNA of most genes in animals, plants, and other eukaryotes contains too much information. The extra segments of largely useless information were named introns, and they must be cut out of RNA before the protein is made. Exons are the portions of the gene that remain in the RNA after the introns have been removed.
- Relics of Eden
At every turn evolutionists are faced with inventing yet another story. But that’s ok because, to paraphrase dazz, they are used to it by now.
At some point in some lineage in the history of life it must have been advantageous to insert crap into the genome. But that’s simply not allowed, under the central dogma. Even so, some mechanism must have evolved to make it possible to insert crap into the genome, and then yet another mechanism evolved to remove the crap from the DNA so that protein could still be produced from genes in spite of the fact that genes had become filled with junk.
At some point, the evolutionary story stretches credulity.
Assume a gene without an intron. Now imagine a scenario in which some piece of crap of indeterminate length gets inserted into that DNA sequence. Imagine more than one. Imagine that protein manufacture continues unabated in spite of the insertion. Imagine now an imaginative mechanism arises to excise the crap out of the gene. Let your imagination run wild!
It’s simply difficult for me to believe that “it just happened, that’s all” is rational. It throws rationality, and science, out the window.
What is the most recent and the most plausible explanation for the rise and fall of introns?
The stcordova model of retroelements: Understand that every single intron, or fragment of it, every transposon or associated element or regulator, every single ERV fragment and insertion, would get it’s own epicycle in Sal’s “model”. Not because anything predicts or explains why it would be so, it’s just something he invents ad-hoc so he can fit it to a young Earth life-created-recently-and-in-perfect-state presupposition.
And repeat it for every single species in existence. Millions of new epicycles for every organism. LOL.
And remember that evolution is bunk unless you can refute every single one of Sal’s ad-hoc rationalizations. And when you do, he will come up with more of them.
A pictorial representation of evolutionary theory!
Beg pardon?
Looks suspiciously like universal common descent.
Below are two articles that discuss the early appearance of mitochondria in eukaryotes. Both take it for granted that mitochondria were produced by endosymbiosis.
Mitochondrion-related Organelles in Parasitic Eukaryotes
Hydrogenosomes, Mitochondria and Early Eukaryotic Evolution
So the data suggest that mitochondria like organelles were a part of the very first eukaryotes.
The following is from a site that challenges the endosmbiotic theory:
A eukaryotic origin of mitochondria
This site also has a short section on the relationship of introns to the mitochondria question here.
Are any of the skeptics here skeptical of the endosymbiosis theory of mitochondria
Just us real skeptics 😎
stcordova,
Sure Sal. That’s what you think, that’s what you think.
stcordova,
The OP was about the origin of introns. You wish only to discuss modern introns – and only then, mostly one goddamned species. Introns are everywhere in Eukarya. So it seems reasonable to try and establish some general principles – rather than saying “look how much I can Google about human introns”.
Frankie,
Yep, just those that think “Gee, they look like bacteria” to be an adequate summary of the evidence.
CharlieM,
Wow! An anonymous article on an anonymous web site. Can’t get any more authoritative than that, eh?
CharlieM,
Not I. I think it has considerable evidential support. I am not sure why one would prefer the idea that bacteria are escapees.
Sure. I don’t take much of things so far removed in time as “gospel truth”. There are degrees of skepticism though. I know this isn’t saying much, but I believe in the endosymbiosis theory for the origin of eukaryotes and mitochondria more than I believe anything Donald Trump says.
What else is there? Sure the “looks like prokaryotes” extends down to genome, but that is still al it is.
And the escapee scenario isn’t the only scenario. In a design scenario it would be a designed marriage- a purposely stripped-down version of a prokaryote used to power the much larger eukaryote.
Rumraket,
Chortle!
It’s an application of Hamilton’s Rule – because of genetic relatedness, a replicator may forego its own direct reproduction to help another – the genes get passed on either way. But it can’t work with 100% relatedness, otherwise bacterial sisters would always be helping each other.
If every cell remained capable of reproduction on its own account, there would be no incentive to forego that reproduction in favour of becoming a somatic cell while a germline relative reproduces your genes on your behalf. Plus, remaining reproductively competent interferes with specialisation.
But with a sexual haploid-diploid cycle, the dynamic changes. Cells can specialise in different roles, one such role being gamete generation itself. Genes in somatic cells get out only through that bottleneck, and are therefore selected to co-operate as a cohesive and differentiated soma, protecting the germline.
By the way Rumraket, one chapter in the book The Origin and Evolution of Eukaryotes is Origin of Spliceosomal Introns and Alternative Splicing.
I’m sure it’s as good as any of the articles Larry listed. One of the authors of that chapter is Scott William Roy, who you will find in Larry’s list of articles.
Another chapter is Origins of Eukaryotic Sexual Reproduction.
It’s a cool book. Don’t assume that because I’m an IDiot I’m also an imbecile. 🙂
Well the author’s name is all over the site, Albert DG de Roos. Here are links to a couple of his articles:
Conserved intron positions in ancient protein modules
and
Origins of introns based on the definition of exon modules and their conserved interfaces
Here he critiques a paper, Analysis of Ribosomal Protein Gene Structures: Implications for Intron Evolution (Yoshihama et al., 2006). He begins:
When I came across his site I wasn’t looking for an authority, I was looking for information and research on the origin of mitochondria. The consensus seems to be that they arose by endosymbyosis. He was arguing against this. I am looking for criticism of his writings. Do you have any?
Are there any other kind, aren’t all introns equally modern?
Let’s say I wanted to study ancient introns. We’ll assume that the ancient ones are the ones shared by all eukaryotes. How do we find them? Do we look for genes that are shared by all eukaryotes and examine them for intra-genic sequences?
How many intron databases are there? How complete are they?
http://bpg.utoledo.edu/~afedorov/lab/eid.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC102483/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC99089/
http://genome.crg.es/cgi-bin/u12db/u12db.cgi
https://www.hsls.pitt.edu/obrc/index.php?page=URL1150311388
Again, procariotes can’ achieve multicellularity because they are procariotes. Very clear.
https://www.researchgate.net/profile/Albert_De_Roos/topics
So back to the reason for the OP. I’m reading a book, Relics of Eden, where I am going to find evidence for evolution. There’s a chapter, “Darwinian DNA” in which the author takes aim at introns, characterizing them as …
“…extra segments of largely useless information…”
“…segments of DNA that contain mostly meaningless sequences of bases … gibberish …”
“They are not cut out of DNA and thus are passed on from generation to generation…”
“…most mutations in introns are selectively neutral…”
All of this is supposed to allow us to create phylogenetic trees based on this “junk” which are supposed to give us a better view of common ancestry than we can get from the exons, and this is evidence for evolution.
Of course, the immediate questions that came to mind werre, if they were useless, why were they favored? If they weren’t favored, what led to their proliferation in the population? If they were selectively neutral, as the author claims, why were the got rid of in procaryotes?
Am I the only one to sense an underlying contradiction?
There are some good clues. If you try phylogenetic analysis on the mitochondrial genome, its closest relatives are endocellular parasites. The ur-eukaryote was presumably single-celled and not colonial, so there wass no such thing as a germ line/soma division.
The mitochondrion got its second membrane because all its bacterial relatives that do aerobic respiration have two membranes.
Mitochondrial genes, and even whole mitochondrial genomes, get pasted into the nuclear genome all the time. They’re called numts, and they’re fairly easy to find. In fact they’re a bit of a nuisance when you’re trying to amplify and sequence mitochondrial genes.
All this should have been easy enough for the author, and you, to look up.
Junk stacked on junk. Introns apparently attract Alu elements.
“…a transposable element stuck in an intron is selectively neutral because the cell removes the intron…”
Or not,
“Transposable elements are just as likely to insert themselves into the protein-encoding parts of a gene as any other part.”
But when that happens, that shit doesn’t survive because it’s a bad insertion!
“But when they do enter the protein-encoding region, they disrupt the genes function, often with dire consequences…”
Follow the logic. Insertion of a transposable element into a coding region is bad. But insertion of an intron into a coding element is, meh, no big deal.
In the first case evolution has simply not managed to solve the problem of inserting crap into a coding region, but in the second case, evolution managed to come up with an elegant solution to the problem of inserting crap into a coding region.
Can’t we have our cake and eat it too?
Too bad John has me on Ignore, because I bet this is all right up his story-telling alley. 🙂
Frankie,
Can you summarise the evidence in a way that doesn’t look deliberately ignorant?
Mung,
Sure, so if you want to understand intron evolution, you don’t just look at one modern one at a time, and apply that function across the board as THE reason they are there. You look for general principles and commonalities among the data you have.
The paper I linked the other day gives one approach. Surveying genomes for distinctive signal of the structure of interest, one can infer when in evolution a particular clade gained a particular commonality.
Much harder to get to the why, of course, because at the moment something arrives in a clade, it’s an unknown species in an unknown local environment under unknown constraints. But I think ‘selfish’ hypotheses have merit. If an element can spread genomically and can yet avoid causing harm to a host, it can persist, and be retained by descendants. This does not preclude the subsequent ‘domestication’ of a particular element copy – it’s little different from mutation in that. Mostly bad, some neutral, some fewer beneficial. Which are we most likely to see, a few generations down the line?
There’s a lot of it about. If you want your bookshelf to look even more impressive in photographs, I would recommend Genes in Conflict by Burt and Trivers.
But broadly, the fantasy peddled by everyone on the ‘anti’ side that evolution proceeds only by adaptation is … a fantasy.
Mung,
How do you get rid of them?
Their mode of transfer. If an element can copy-paste or cut-paste itself (steady now … just an analogy … ) it can spread. Particularly if the species indulges sex, which is notoriously unhygienic. When 2 genomes reside in the same cell, they can much more readily jump from one lineage to another, where in an asexual line they are pretty much confined to desultorily hopping round the same set. And in that scenario, their detriment becomes much more rapidly apparent.
Prokaryotes are under a much more severe mechanistic constraint than eukaryotes. The former can acquire nutrition and energy only by diffusion; the latter can eat. They chuck the molecules of their prey at their mitochondria, which fall on it like a pack of dogs and generate ATP by the bucket load. They use the rest to build their cells, that are up to 50,000 times bigger than a bacterium. They have a different energy-and-materials budget.
Prokaryotes have to work their asses off just to keep up with the rest. Any slowdown of growth, or requirement for extra energy and molecules, is quickly swamped by the unmutated remainder.
Eukaryotes, meanwhile, gained leisure. And with each enhancement, they generated more opportunity for genomic parasites to spread, as material and energy costs of DNA/RNA became less and less a proportion of the total budget.
What’s a junk-laden eukaryote competing with? Other junk-laden eukaryotes. How did they all get so junk-laden? Incrementally. No one 300-base addition is particularly deleterious.
It’s down to mechanistic differences and ecology, in short.
Mung,
Yep, with you so far.
That too is true. There is a mechanistic bias towards genes because the intergenic regions are more likely to be buried in heterochromatin. Transposon action requires access to DNA. But given that access, it can go anywhere – promoter, exon, intron.
Well, yes.
I have. And I don’t see the problem you are getting at.
One wonders why someone who has to have it all explained to them thinks they then have a right to be “skeptical” about things they clearly don’t understand.
Mung, it’s not that you are skeptical, it’s that you are ignorant. And I mean that in a simply factual way. It’s not an insult. It’s just a fact.
I see that you missed the point. So you behaved exactly how I expected, which is why I didn’t bother giving an explanation in the first place.
They weren’t favored by the host, they are essentially parasites. But they’re selfish genetic elements, they follow their own evolutionar trajectory.
There’s an arms-race between the host and the introns. The introns are always a step ahead, they replicate and insert themselves all over the place, much more than the host does. Sorta like we’re perpetually haunted by influenza and the common cold.
Though, their negative effect on fitness is very low. So even though they’re deleterious, it’s very very weak. Meaning population sizes would have to be absolutely colossal for selection to overwhelm drift and be effective at weeding them out. Meaning you’d only expect selection to have weeded them out in species with very very large effective population sizes. Like bacteria. That’s what we find. Almost no bacterial species have introns, and almost all large, multicellular eukaryotes have them.
There are grey-areas and crossover zones, where the type of intron and it’s method of proliferation, in combination with a unique lifestyle of the host, allows it to persist where you’d have otherwise guessed it should be gone (and the reverse of course, there are situations where you’d expect it to have persisted, but in actuality is gone). That’s biology for you. You find a general case, and then somewhere in some rare, obscure and unusual situation, something defies your general expectation. That doesn’t mean the general expectation is completely false, it just means there are unique exceptions.
They’re not favored by the host, but when population sizes are small (as they usually are in large multicellular populations), selection is weak and so they can proliferate relatively inhindered.
You must distinguish betwee mutations in introns, and the intron itself. Introns are not selectively neutral (though nearly so). Mutations in introns that don’t affect the splicing sites, are neutral.
If you read more carefully, you would have caught the distinction between mutations IN introns, and the entire intron itself, as the author you quote made clear.
Those two things aren’t in contradiction. An intron is not a protein-coding part of a gene. So a transposable element stuck in an intron, is not the same thing as a transposable element stuck in a protein-coding region (called an exon).
There are introns and exons. Roughly speaking, introns are generally junk, exons code for protein.
A transposable element inserting in an intron, is not inserting in a protein-coding part of a gene. IOW, an insertion in an intron, is not an insertion in an exon.
Mung. Read your book for comprehension, and more carefully. Otherwise this is what we get. You come here with something you failed to understand, and then end up looking like an idiot desperately looking for crap you can quote and point and laugh at. But what really happened? You failed to comprehend what you read.
Because transposons can’t remove themselves prior to translation. They can’t splice themselves out. Introns can.
Intron =/= transposon
Transposons can insert IN introns. And they can insert in coding elements.
So can introns, but they can remove themselves from mRNA (or get removed by the spliceosome) before translation happens.
Neither introns, nor transposons can remove themselves from chromosomal DNA. So once it’s there, it’s stuck. But once transcribed into RNA, the difference between introns specifically, and transposons of all types, become clear. Introns can cut themselves out of the RNA, before it goes on to be translated. Transposons cannot.
Because it can cut itself out, once that coding element has been transcribed into RNA.
If you read for comprehension, you can have all the cake you want.
Why don’t YOU, Allan? Then tell us how to test the claim that one prokaryote engulfed another and badda-bing, badda-boom- mitochondria! Please put it in terms of blind and mindless processes.
Or admit that you can’t and yours isn’t a scientific claim
Rumraket,
Personally, I think the mechanistic differences probably swamp any population size effects, when going between kingdoms. I know the way you’ve presented it is fairly common, and due to Lynch, but I’d say it’s the difference in the selection coefficients themselves, per n surplus bases, rather than the effectiveness of selection on the same s, that marks the eukaryote/prokaryote distinction.
The two aren’t mutually exclusive, of course.
LoL! And those junk-laden euks just happened to evolve histone octamers for spooling all of that excess DNA- active spools at that! It’s as if evolutionism posits magic as a mechanism
There isn’t an “anti” side when it comes to mere evolution.
Too bad for you
The easiest reason is that there are very many anaerobic bacteria that show no indication of ever having been aerobic, while mitochondria are aerobic and chloroplasts are oxygenic photosynthesizers.
If bacteria evolved from mitochondria and/or chloroplasts, they’d have the evidence of having been derived from them. Obligate anaerobes would be rare among bacteria, at most, and even those would likely have indications of having been aerobic and/or oxygenic once. But mitochondria and chloroplasts only sample a very small amount of the diversity of bacteria (not just with respect to oxygen, of course), so would seem to be endosymbiotic organelles coming from aerobes and cyanobacteria.
Then comes the problem of dependent and controlled organelles becoming independent, even if one allows that mitochondria and chloroplasts apparently had far more genes once (could be that it was adaptive for controlled organelles to have many genes, but even then they’d likely be controlled in a manner that would make becoming independent difficult). But that’s been covered.
Glen Davidson
Frankie,
Enough with the equivocation. You know damn well what I mean.
Frankie,
Hey! Here’s a thought. Maybe it didn’t have to happen that way round …
LoL! The equivocation is all yours- tat was the point
Maybe it didn’t happen at all- there isn’t any way to test the claim blind and mindless processes didit
Hey thanks! Ordered.
Allan and Rumraket, appreciate the comments. Good stuff. Thanks.
Rumraket, you might consider that you don’t understand what I wrote, rather than assuming I didn’t understand what I read. I was making an argument by analogy, which means I understand the difference between introns and TEs.
Frankie,
Yet strangely, I strive to be clear. Dis make me sad. 🙁
GlenDavidson,
I wasn’t saying that bacteria could have evolved from present day mitochondria or chloroplasts. I was looking into the possibility that bacteria may have come from ancient protists, eukaryote precursors or the organelles thereof. I believe that there are some mitochondrion-related organelles which respire anaerobically.
Anyway maybe this is a conversation for some other time. Much as I’d love to carry on with the discussion on mitochondria I feel that I have veered off topic with these questions.
Okay and fair enough, but that just leaves me confused because, if in fact you had made the misreading I understood you to have made, your belief that there was a contradiction would have made sense.
If in fact you understood it, I don’t see why you would have thought there to be a contradiction.
I see a couple. Here’s the first.
Assume procaryotes were the precursors to eucaryarotes. Allegedly the common ancestors of procaryotes and eucaryotes had introns. Following the same reasoning for introns being lost in procaryotes, they should have been lost in the lineage leading to eucaryotes, they should have been lost in the common ancestor.
To say otherwise is to turn the whole lost in procaryotes but retained in eucaryotes into just so much ad hoccery. Like I said, trying to have the cake and eat it too.
What is needed is an argument for why introns would be lost in procaryotes but retained in the common ancestor. Can you think of an argument in favor of how introns were lost in procaryotes that can’t also be applied to the common ancestors of procaryotes and eucaryotes? Why did intron loss in procaryotes wait until after the two lineages diverged? Why not before?
and
This is like a car designer saying that all the instructions for the materials needed to build a car are necessary, but the instructions which enable the components to be assembled correctly and maintained in service are generally just junk!
In a talk which is well worth listening to, according to John Mattick, most of our protein coding genes we have in common with creatures such as c elegans. By and large the parts set for animal development has been around for hundreds of millions of years. So he asks the obvious question: Where is the information that programs the complexity? It was discovered that most of our genome is transcribed into RNA in a dynamic manner in different cells and tissues at different stages of development. At the time Mattick was disappointed that so many working in his discipline, instead of saying “this is interesting”, just assumed it was noise and thought no further about it.
From what I can see the numbers of introns equate fairly closely to the complexity of the animal.
Here is an interesting paper on introns:
Surprisingly high number of Twintrons in vertebrates