Introns

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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?

302 thoughts on “Introns”

  1. Mung,

    I recently viewed the movie Interstellar. I guess I could identify with the Coop, pushing books out of a bookshelf on to the floor in an attempt to communicate with the “real” world where his daughter was.

    I watched it on Saturday night. The hero travels into a black hole and lives to tell. What a stud 🙂

  3. So let’s run with the idea that introns existed in a common ancestor and were lost, presumably because to lose them was beneficial in some way in speeding up reproduction due to having less DNA to copy during cell division.

    What must we also believe, in order to believe that?

    For example, we would need to believe that the common ancestor of procaryotes and eucaryotes, itself, presumably, a procaryote, was slower at reproducing than the later prokaryotes.

    We would also need to believe that this ancestral lineage failed to stumble across this improvement until after the eucaryote split.

    We must also believe that introns can’t actually speed up reproduction. Perhaps they can. Or maybe it was just luck of the draw.

    We must believe that there was a way to lose the introns. Some mechanism, perhaps.

    We must believe that there were no other variables involved, nothing else going on, that it’s a simple case of less DNA means faster reproduction.

    What is the evidence for any of this? Why is this a better story than alternative stories.

    Why not just believe that procaryotes and eucaryotes had separate origins?

  4. colewd: The hero travels into a black hole and lives to tell. What a stud

    Don’t forget about his trusty sidekick, the computer!

  5. Mung: Why not just believe that procaryotes and eucaryotes had separate origins?

    Yes, yes! rubs hands in evil stance YEC is caaaaaaaalling and you know you want it Mungy!

  6. Mung,

    So let’s run with the idea that introns existed in a common ancestor and were lost, presumably because to lose them was beneficial in some way in speeding up reproduction due to having less DNA to copy during cell division.

    Luca was a yeast cell 🙂

  8. Don’t be silly dazz.

    More probable eukaryote fossils begin to appear at about 1.8 billion years ago.

    here

    The late Archean record for eukaryotes is limited to trace amounts of biomarkers. Morphological evidence appears in late Paleoproterozoic and early Mesoproterozoic (1800-1300 Ma) rocks.

    here

    Not exactly in keeping with a 6000 yer old earth.

  11. colewd: This makes me skeptical of the age of the first keg of beer.

    All beer shares a common ancestor. You can’t fight science.

  12. Alrighty then. Hitting the books:

    In this section we describe the evolutionary history of introns since LECA.

    – The Origin and Evolution of Eukaryotes

    Assume the existence of introns. Not exactly an explanation for when, how, or why introns arrived on the scene in the first place. More study required.

  13. …spliceosomal introns appeared abruptly at the time of the origin of eukaryotes…

    Oh goody. Creationists just love abrupt appearance.

  15. Mung: All beer shares a common ancestor. You can’t fight science.

    Technically, drinking a beer is the same thing as murder.

    I mean really, where do you draw the line between a human and yeast? Just because a yeast didn’t give birth to a human directly, what’s next, drinking people from West Virginia because they are somehow less evolved?

  16. Mung:
    So let’s run with the idea that introns existed in a common ancestor and were lost, presumably because to lose them was beneficial in some way in speeding up reproduction due to having less DNA to copy during cell division.

    What must we also believe, in order to believe that?

    For example, we would need to believe that the common ancestor of procaryotes and eucaryotes, itself, presumably, a procaryote, was slower at reproducing than the later prokaryotes.

    We would also need to believe that this ancestral lineage failed to stumble across this improvement until after the eucaryote split.

    We must also believe that introns can’t actually speed up reproduction. Perhaps they can. Or maybe it was just luck of the draw.

    We must believe that there was a way to lose the introns. Some mechanism, perhaps.

    We must believe that there were no other variables involved, nothing else going on, that it’s a simple case of less DNA means faster reproduction.

    What is the evidence for any of this? Why is this a better story than alternative stories.

    Why not just believe that procaryotes and eucaryotes had separate origins?

    Well, one could just take the fantastical approach of Larry Moran, and just say that every novel change that has come along wasn’t beneficial at all!

    Mutations spiraling out of control just so happened to form some sophisticated systems. What’s so hard to believe about that? It certainly doesn’t mean any of it was beneficial!

    Give blind luck a little bit of credit, won’t ya?

  17. colewd,

    What do you think caused the proliferation of introns inside DNA? Introns that had the ability to precisely remove themselves.

    Good grief. Precisely that!

    Disruptive introns would damage their hosts, and so do not remain to be boggled over. Non-disruptive introns can proliferate. It’s just selection vs magic all over again. Creationists appear unable to understand selection, so magic it is.

  18. Mung: So let’s run with the idea that introns existed in a common ancestor and were lost

    Why? The common ancestor of what?

    If they were lost, why would they still be around in basically all eukaryotes?

    You’re asking, why aren’t they in prokaryotes when they are in eukaryotes? Did you read any of the articles Larry linked?

    We must believe that there was a way to lose the introns. Some mechanism, perhaps.

    There is. It’s called deletion. One of many types of spontaneous mutations that can happen, is deletion of nucleotides. By some mistake of the copying apperatus during replication, some nucleotides are “skipped”. This is an observed fact. This is how E coli in the LTEE threw away a lot of it’s no longer necessary genes in the simple and constant flask-environment and why it replicates in basically 20 minutes now, instead of about an hour.

    We must believe that there were no other variables involved, nothing else going on, that it’s a simple case of less DNA means faster reproduction.

    We must believe this for what? The lack of introns in prokaryotes? Then we have a simple experimentally proven, observational fact to contend with: It is the case that less DNA means faster reproduction. And it is the case that making lots of extra DNA costs energy.

    What is the evidence for any of this? Why is this a better story than alternative stories.

    Because of the nesting hierarchical arrangements in the distribution of introns, intron-like sequences and the mechanisms by which they excise themselves and get excised from mRNA sequence.

    Why not just believe that procaryotes and eucaryotes had separate origins?

    Because that hypothesis can’t explain the data without having to invent a host of additional ad-hoc explanations, with no observational basis. There are too many homologous structures and sequences in prokaryotes and eukaryotes for their independent origin to be the most plausible explanation.

    At minimum you’d have to invoke an inordinate amount of LGT between them. Not a very plausible scenario.

    It’s not that that couldn’t have happened, it’s that it is an even worse explanation if you want to account for all the data (not just look at introns in isolation).

    There’s a much more simple, more plausible mechanism, which we know exists from direct observation, that can account for all these similarities and their patterns of divergence over time: Vertical inheritance with mutations. Descent with modification. Parents give birth to offspring, and the offspring inherit their parent’s genes with a few mutations here and there. Some of those mutations are duplications, some are point mutations, some are insertions, some are deletions.

  19. stcordova,

    But since Allan is sick of me listing the facts, perhaps I’ll spare him and you.

    I’m sick of obfuscating detail. The role of a specific intron is like the role of a specific mutation – it does not tell you about mutations in general. It tells you about that mutation.

    Unless there is some general class of functions common to all introns, in all species that have them, some detail of a role specific to some self-obsessed primate species is individually interesting, but not helpful for understanding the whole, or its evolution outside of humans. We could spend years chasing sticks, unable to see the forest.

  20. stcordova,

    On the other hand, since I have a small fan club of 3 people here at TSZ, maybe I might treat them to some more facts

    Because of course they have no means of finding facts otherwise!

  21. J-Mac,

    Or should I give you many examples in question?

    Oh, yes please. Stuff your post with ’em. Big long lists of Things Evolution Don’t Explain, across as many disciplines as poss. Cheers.

  22. Mung,

    Why not just believe that procaryotes and eucaryotes had separate origins?

    Multiple lines of evidence argue against this. Which I believe one of your colleagues is about to summarise as “well, they look like prokaryotes so…”.

  23. Mung,

    So let’s run with the idea that introns existed in a common ancestor and were lost, presumably because to lose them was beneficial in some way […]

    For example, we would need to believe that the common ancestor of procaryotes and eucaryotes, itself, presumably, a procaryote, was slower at reproducing than […]

    We would also need to believe that this ancestral lineage failed to stumble across this improvement […]

    You seem in general to be running away with the idea that things only happen in evolution if they are beneficial – and only to the organism, at that. I think you probably know better, but when caricaturing, suddenly, that’s the version of evolution you go after.

  24. Mung: Alrighty then. Hitting the books:

    In this section we describe the evolutionary history of introns since LECA.

    – The Origin and Evolution of Eukaryotes

    Assume the existence of introns. Not exactly an explanation for when, how, or why introns arrived on the scene in the first place. More study required.

    Yes. Some times we don’t know, because the data available at the time does not lend itself to us being in a position to claim that we know. Frustrating when you want to know that thing we don’t know, but such is life.

    Regardless, Larry linked a large number of good papers on this earlier in the thread. Did you read them?

    This one, for example, is good and quite extensive:
    Rogozin, I. B., Carmel, L., Csuros, M., and Koonin, E. V. (2012). Origin and evolution of spliceosomal introns. Biology direct, 7:11. [doi: 10.1186/1745-6150-7-11]

    Origin and evolution of spliceosomal introns: a synthetic concept

    The evidence presented here and elsewhere [42, 45, 53, 62, 84] supports a ‘numerous introns early in eukaryote evolution’ view. The discovery of introns in jacobids [278] and other excavates [4, 5] is compatible with this concept. Even more strikingly, approximately 60% of the introns in the parabasalid Trichomonas vaginalis occupy the exact position of an intron in an orthologous gene from at least one other eukaryotic lineage [279], and similar observations have been made for the free-living excavate Naegleria gruberi[6]. Most importantly, probabilistic reconstructions of intron gain and loss provide consistent and by now compelling evidence that ancestral eukaryotic forms including the LECA possessed intron-rich genes, with intron densities comparable to those in the most intron-rich modern organisms such as mammals [53, 141]. These findings have fundamental consequences for our understanding of the evolution of eukaryotes and possibly of the ultimate origin of the eukaryotic cellular organization [46, 280, 281].

    It appears likely that the emergence of the eukaryotic cell or the initial stages of its evolution involved, among other radical innovations, a catastrophic intron invasion (Figure 9) [46]. Structural similarities between the terminal regions of spliceosomal introns and those of self-splicing Group II introns (retro-transcribing elements) leave essentially no doubt in the existence of a direct evolutionary connection between the two classes of introns [282]. Moreover, the elements of Group II introns involved in the autocatalytic splicing reaction apparently also gave rise to the spliceosomal small RNAs [282, 283]. Thus, at an early stage in the evolution of eukaryotes, an irreversible transition apparently took place from autocatalytic splicing to splicing mediated by a universal trans-acting catalyst (the spliceosome). This transition involved the split of the ancestral Group II intron structure into the catalytically inert spliceosomal introns and the catalytically active RNA moiety of the spliceosome that was also accompanied by the degradation of the reverse transcriptase open reading frame within introns [280].

    It appears most likely that the Group II intron invasion was triggered by the establishment of the endosymbiosis between an α-proteobacterium and an archaeal host (Figure 9). Notably, α-proteobacteria typically contain in their genomes a relatively large number of Group II elements compared to other bacteria [284]. Upon the endosymbiont invasion of the archaeal host, the symbiont’s Group II introns might have been ‘unleashed’, in part due to repeated lysis of the symbiotic cells (the evolving mitochondria) [280]. At the fundamental evolutionary-theoretical level, the tolerance of the emerging eukaryotic cell to such an invasion could be potentially explained by a population bottleneck which severely limited the efficacy of purifying selection [50, 280, 285].

    Indeed, it has to be emphasized that Group II introns are typical mobile elements that actively spread around the host genome when given a chance by weakness of purifying selection pressure.

    However, at the mechanistic level, the adaptation of the early eukaryotes to the swarms of genomic parasites (if this is what introns are, Figure 9), which severely compromised the integrity of their genomes, an adaptation that apparently involved rapid evolution of the dauntingly complex spliceosome, remains an intriguing enigma. The intron invasion, probably spawned by the mitochondrial endosymbiont (Figure 9), could have led to a peculiar, intron-dominated genome architecture of the early eukaryotic, with up to 80% of the genomic DNA comprised of introns [286]. This genome structure could be sustainable only under a severe population bottleneck and might have critically contributed to the emergence of the principal features of the eukaryotic cell [46, 286]. The evolution of the signature features of eukaryotic cell organization, such as the endomembrane apparatus including the nucleus, the nonsense-mediate decay system and the ubiquitin system, can all be conceptualized as multiple levels of defense against the deleterious effects of the intron invasion [46, 172]. Furthermore, the early, mobile introns could have triggered the proliferation of multidomain proteins via homologous recombination between introns in different genes. Obviously, most of such events would be strongly deleterious but some might have created potentially useful domain combinations without losing much important information, and thus would be picked by selection. Introns also created the potential for controlled alternative splicing (see above), a mechanism that came to prominence at a later stage of eukaryotic evolution and made a crucial contribution to the evolution of complexity in multicellular organisms. To summarize, the intron invasion that was probably concomitant with the emergence of the first eukaryotic cells can and probably should be envisaged as one of the key factors of eukaryogenesis.

    Evolution of exon-intron structure of eukaryotic genes had been long considered in the context of the “introns-early” vs. “introns-late” debate [39, 40, 41, 42]. Although the original introns-early idea is hard to reconcile with the absence of spliceosomal introns (and the spliceosome itself) in prokaryotes and the absence of conserved intron positions in ancient eukaryotic paralogs (Figure 8) [148], this concept can be easily restated in more realistic (even if less dramatic) terms. Specifically, the entirety of the observations discussed above, strongly suggests that the spliceosomal introns originated from self-splicing Group II introns which invaded eukaryotic genes (or perhaps more precisely, genes of the archaeal host of the proto-mitochondrial endosymbiont) concomitantly with or at the latest shortly after the origin of the eukaryotic cell. As indicated by evolutionary reconstructions, subsequent evolution involved mostly lineage-specific loss of introns punctuated with a few episodes of new gains. Under this scenario, although there is no evidence of existence of modern-type spliceosomal introns (or spliceosomes) prior to the origin of eukaryotes, their ancestors were ancient mobile elements that probably co-existed with cellular life forms throughout their evolution or possibly even antedated modern cells [287]. Thus, although the ‘exon hypothesis’ and the original idea that the first genes contained multiple introns do not seem to be supported by any evidence, the evolutionary lineage leading to spliceosomal introns indeed could be as old as some of the first replicating genetic entities.

  25. Mung,

    Assume the existence of introns. Not exactly an explanation for when, how, or why introns arrived on the scene in the first place. More study required.

    What we should do is proclaim that the designer did it and leave it at that. Do you agree?

  26. Allan Miller:
    Mung,

    You seem in general to be running away with the idea that things only happen in evolution if they are beneficial – and only to the organism, at that. I think you probably know better, but when caricaturing, suddenly, that’s the version of evolution you go after.

    Right. Who says lungs were always beneficial? Maybe they are useful now, because they got co-opted, but probably they were just neutral for a long time.

    Heck, it doesn’t kill you to have something to breathe with, and then eventually some animals just started actually using those windbags that they had laying around.

    And since they happen to convert the oxygen into the blood cells, that was darn convenient. Plus a diaphragm muscle finally figured out how to be useful for something.

    From neutral to beneficial in just a few easy steps. Like if you have a junkyard full of a bunch of discarded parts, it doesn’t take a genius to make something out of them. It doesn’t even take a plan. Just some wind!

  27. OMagain:
    Mung,

    What we should do is proclaim that the designer did it and leave it at that. Do you agree?

    No no, if “nature just does it”, its just giving “nature” a name, that’s all.

  28. Introns, exons and the mechanism of splicing have a real utility in multicellular organisms where you need different tipes of the same protein at different times and cells of the same organism. Finding them in the LECA is a point for the “front loading” of evolution. Eucariotes exist in order to develope multicellularity.
    Why there is no multicellular procariotes?

  29. Has anyone read the papers Larry linked to? They are not only full of speculation they also fail the Judge Jones litmus test- not one paper [pays homage to blind and mindless processes (Jones dismissed the claim that ID has peer-reviewed support because the papers didn’t mention ID).

    It is strange what evos will accept as evidence for their position even when the evidence doesn’t support it

  30. No one in ID says to just proclaim the designer didit and ;eave it at that. Talk about humping a straw man.

    ID is about the detection and study of design in nature- just like archaeology and forensics.

  31. Did eukaryotes evolve from prokaryotes or did prokaryotes evolve from eukaryotes?

    Can evolution make things less complicated?

    Instead, the data suggest that eukaryote cells with all their bells and whistles are probably as ancient as bacteria and archaea, and may have even appeared first, with bacteria and archaea appearing later as stripped-down versions of eukaryotes, according to David Penny, a molecular biologist at Massey University in New Zealand.

    Penny, who worked on the research with Chuck Kurland of Sweden’s Lund University and Massey University’s L.J. Collins, acknowledged that the results might come as a surprise.

    “We do think there is a tendency to look at evolution as progressive,” he said. “We prefer to think of evolution as backwards, sideways, and occasionally forward.”

    OK if euks aren’t a union of proks AND if euks were first on the scene (in any evolutionary senario), abiogenesis just got a bit more difficult to explain. And if life didn’t arise from non-living matter via unintelligent, blind/ undirected (non-goal oriented) processes, there is no reason to infer its subsequent diversity arose solely via those type of processes.

  33. Blas: Introns, exons and the mechanism of splicing have a real utility in multicellular organisms where you need different tipes of the same protein at different times and cells of the same organism.

    There’s very very few cases of this actually happening. Mostly, alternative splicing causes disease.

    Finding them in the LECA is a point for the “front loading” of evolution.

    Fron loading is ad-hoc and fails to explain the actual distribution in eukaryotes, including the distribution of similarities in the structures of the spliceosome.

    Eucariotes exist in order to develope multicellularity.

    In-order-to? Cool just-so story bro.

    Any idiot can just sit back and claim that whatever happens, happens because it has the purpose of giving rise to what happens next.

    The fact that one event that happens later, is dependent on an event that happened before, does not entail that the previous event was meant to make the later event happen.

    Why there is no multicellular procariotes?

    They can’t become multicellular without endosymbiosis. Hence, eukaryotes.

  35. Rumraket,

    They can’t become multicellular without endosymbiosis. Hence, eukaryotes.

    I would suggest that they also can’t become multicellular without sex [eta: our kind, not theirs]. Which is also an important dynamic for the spread of selfish elements.

  36. Rumraket: They can’t become multicellular without endosymbiosis. Hence, eukaryotes.

    Just a quick question as its all I have time for at the moment.

    I would genuinely like to know how it is determined that certain organelles are the result of endosymbiosis and that it was not the other way round. How do we know that bacteria are not derived from escaped cells which originally belonged to eukaryotes?

    What evidence do we have either way?

  37. CharlieM: I would genuinely like to know how it is determined that certain organelles are the result of endosymbiosis and that it was not the other way round. How do we know that bacteria are not derived from escaped cells which originally belonged to eukaryotes?

    What evidence do we have either way?

    Good question, and I don’t remember exactly. Don’t take my personal ignorance as an indication of the state of the field though. I’m quite sure I’ve read something about that a few years ago. I think it mostly has to do with parsimony. In order to make the eukaryotes-first view “fit”, you have to invoke a host of additional ad-hoc hypotheses to explain the distribution of genes, structures and so on, in prokaryotes vs eukaryotes. Don’t take my word for it, I don’t remember where I ran into this.

  38. CharlieM,

    Yes, parsimony. There are quite a few things to account for that require far less appeal to special circumstance if the route is prokaryote -> eukaryote. For example, the nuclear genome contains many genes that appear, on grounds of homology, to have migrated from the mitochondrion. For such an organelle to escape in its presently highly reduced state would require a substantial set of those genes to go the other way – to migrate from the nucleus – but only those genes that would support an independent lifestyle. It is unlikely.

    If, on the other hand, one imagines ancient mitochondria to have been more self-sufficient than modern ones, and therefore more capable of being able to make the transition to free-living, there seems little reason for them to be so – unless they were, in fact, recently enclosed bacteria.

  39. Allan Miller: I would suggest that they also can’t become multicellular without sex [eta: our kind, not theirs]. Which is also an important dynamic for the spread of selfish elements.

    I don’t understand sex very well and I need to read more about it.

    How’s that for quote-mineable sentence of the century? 😀

  40. J-Mac:
    The is supposed be The Skeptical Zone but the body of skeptics in charge of the TSZ are only skeptical about the ID… How is this fair name for this blog? Why didn’t they callit “The ID Skeptical Zone”? It would be more accurate.
    Has anyone seen one of the TSZ promoters being skeptical about their own beliefs, like evolution or OOL?
    I doubt that very much…

    The tools of skepticism are available to everyone. Be the change you want to see.

    Before you do, though, make sure you understand that arguments from personal incredulity are not in the skeptic’s toolbox.

  41. Patrick: Before you do, though, make sure you understand that arguments from personal incredulity are not in the skeptic’s toolbox.

    And yet that is all you and yours have.

  42. There isn’t any way to scientifically test the claim that eukaryotic organelles like mitochondria and chloroplasts were once free-living prokaryotes. So that would be a problem for the hypothesis.

  43. Patrick: The tools of skepticism are available to everyone. Be the change you want to see.

    Should we do as you say or should we do as you do? For example, I don’t recall accusing anyone here of being a child abuser.

  44. My dear Rumraket, Larry wrote:

    Larry Moran: I can understand why the origin of introns might seem impossible to people who haven’t learned (or don’t bother to learn) basic biochemistry and molecular biology.

    So I’m hitting the books first to see what they say. If it turns out that the books don’t cut it when it comes to intron evolution I’ll move on to the papers. But I want to hit the biochem and molbiol textbooks first because I want to see if there’s any substance to Larry’s claim.

  46. Allan Miller
    I’m sick of obfuscating detail. The role of a specific intron is like the role of a specific mutation – it does not tell you about mutations in general. It tells you about that mutation.

    I don’t see it that way. The characterization of the genome function in 3 dimensions vs. the usual 1 dimensional approach as evidenced the Wells vs. Moran-Matheson-Hunt 2010 debate is an example of inaccurate thinking that is now getting cleared up because we have experiments like 3C, 4C, 5C, 6C and High C. I put it on the table. It’s tiresome you guys never mention it, much less address how it came to be. I was the first to put the stuff on the table at TSZ starting with slides from Wesley Pikes presentation at ENCODE 2015 which I had the honor of being a part of. I provided a diagram highlighting Pike’s work here last year:

    Philosophy and Complexity of Rube Goldberg Machines

    What I put on the table is the latest and best, and his hardly obfuscation.

    Unless there is some general class of functions common to all introns, in all species that have them, some detail of a role specific to some self-obsessed primate species is individually interesting, but not helpful for understanding the whole, or its evolution outside of humans. We could spend years chasing sticks, unable to see the forest.

    Why does there have to be some general class of role for introns? Any eukaryote that has a 3D Origami code may have a different Origami code and use for intron different from another creature.

    I pointed out the primate specific Alus often come in mirror-image pairs like punctuation marks (an amazing thing in and of itself), and they often encompass introns, and then these Alu-capped introns are then transcribed into circular double-stranded RNAs that are a mechanism for alternative splicing and who knows what else.

    The introns-are-junk crowd are arguing from ignorance, and when I actually start citing relevant laboratory experiments to the contrary, I get a wall of nay-saying and resistance, like DNA_Jock and John Harshman suddenly having inability to do elementary math like knowing the difference between 0.1% and 1.5%.

    Let the readers see these primate specific use of introns, which I put on the table at TSZ in the following discussion which I’ll highlight:

    Some evidence ALUs and SINES aren’t junk and garbologists are wrong

    Examination of the human transcriptome reveals higher levels of RNA editing than in any other organism tested to date. This is indicative of extensive double-stranded RNA (dsRNA) formation within the human transcriptome. Most of the editing sites are located in the primate-specific retrotransposed element called Alu. A large fraction of Alus are found in intronic sequences, implying extensive Alu-Alu dsRNA formation in mRNA precursors. Yet, the effect of these intronic Alus on splicing of the flanking exons is largely unknown. Here, we show that more Alus flank alternatively spliced exons than constitutively spliced ones; this is especially notable for those exons that have changed their mode of splicing from constitutive to alternative during human evolution. This implies that Alu insertions may change the mode of splicing of the flanking exons. Indeed, we demonstrate experimentally that two Alu elements that were inserted into an intron in opposite orientation undergo base-pairing, as evident by RNA editing, and affect the splicing patterns of a downstream exon, shifting it from constitutive to alternative. Our results indicate the importance of intronic Alus in influencing the splicing of flanking exons, further emphasizing the role of Alus in shaping of the human transcriptome.

    There you have it. In a discussion of introns, how is this obfuscation? It sound more like “I want to plug my ears because Sal is making a devastating point I can’t handle so I’ll complain about him trying to dazzle rather than inform and claim it’s spamming and obfuscation.”

    Some evidence ALUs and SINES aren’t junk and garbologists are wrong

    From that discussion is a diagram that shows how dsRNA are formed from introns capped at each end by Alus, which are unique to primates, and therefore are unique uses of introns not found in other species.

    From the quotation above, the circular dsRNAs depicted below are often derived from introns. They induce alternative splicing and who knows what else.

    Possible Alu-induced RNA processing events.

    a Inverted Alus on each side of an exon that form a dsRNA structure may induce exonic RNA circularization.

    b An intronic Alu with a mutated or edited sequence can induce alternative splicing and/or Alu exonization.

    c Inverted Alu elements forming a dsRNA structure frequently induce A-to-I editing at nearby sites.

    d Within introns Alus can contribute to maturation of miRNAs.

    e Alu elements in 3′UTRs may act as miRNA targets

    Finally, it’s not me trying to dazzle nay-sayers like you, it’s God himself offering things to dazzle people who are willing to wonder at what He has made. But if nay-sayers want to close their eyes to it and call discussion spam and obfuscation, they can. But I provide the data for people willing to see what God has made, and that He made primates and humans special in the way they use introns.

  47. They can’t become multicellular without endosymbiosis. Hence, eukaryotes.

    Procarites can´t become multicellular because they are procariotes.
    Talking about so stories.

  48. Blas: Procarites can´t become multicellular because they are procariotes.
    Talking about so stories.

    You’d have to actually understand something about what prokaryotes and eukaryotes are, and how this affects their ability to become more complex. But since you aren’t here to learn, just to declare what you believe and what you don’t, it’s not worth my time to explain it. Suffice it to say, it’s obviously not because someone decided to label them “prokaryotes” that prevents them from becoming more complex. It’s about what they are and how they work, not what they are named.

  49. stcordova: Finally, it’s not me trying to dazzle nay-sayers like you, it’s God himself offering things to dazzle people who are willing to wonder at what He has made.

    Cool story bro.

  50. stcordova: Why does there have to be some general class of role for introns? Any eukaryote that has a 3D Origami code may have a different Origami code and use for intron different from another creature.

    And here we have the history of astronomy, recapitulated in molecular biology. Sal has taken the role of the geocentrists, in trying to explain the motion of the planets and distant stars, he needs invoke an ad-hoc epicycle for every object in the universe to try to make it “fit” a model with a stationary Earth at the center.

    So Sal is inventing an ad-hoc hypothesis for every genetic element, in every different species on the planet. Millions upon millions of new hypotheses, that fits nowhere else but the particular element in question, for that one particular species.

    Out the door goes concepts like parsimony, simplicity and explanatory power. Pseudoscience at it’s finest. That is what a conclusion-first, evidence-second method gets you. Epicycles. Millions upon millions of epicycles. For every star, every planet, every asteroid, meteor, galaxy, every grain of dust or lone atom in the void in the entire Cosmos, invent a new orbit that nothing explains, for no other purpose than to make it fit a universe concieved with Earth at it’s center.

    Sal believes in a young Earth with a creator that recently created all life on it perfectl and flawless, so to fit his Human-centric model, he now has to invoke millions upon millions of ad-hoc hypotheses to explain variations in genome size, the patterns in distribution of many different classes of retroelements, of which there are millions in every species. All of them used to be functional, in their own unique way.

    “It can scarcely be denied that the supreme goal of all theory is to make the irreducible basic elements as simple and as few as possible without having to surrender the adequate representation of a single datum of experience.” – Albert Einstein

    “Why does there have to be some general class of role for introns?” – Salvador Cordova

    Of course Sal, there doesn’t have to be. But you know, in science we like things that make sense. I know, how silly.

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