302 thoughts on “Introns”

1. Mung: 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?

   I understand, and that question makes sense. You have to look at it in more detail though. There are many different species of prokaryotes. Specifically, the prokaryotes from which introns are hypothesized to be inherited, alpha-proteobacteria, still have introns today, called group II elements, very similar to group II self-splicing introns found in eukaryotes, and therefore thought to be related to them.

   The alpha-proteobacteria class is thought to be the descendants of the bacterial species that became the mitochondrion (invaded the host archaeal cell as an endoparasite), which resulted in the host archaeal cell basically getting invaded by the introns present in the ancestor of mitochondria. Which again, would have been an alpha-proteobacteria. So basically there was never any loss of introns involved from the prokaryote ancestor. Almost all eukayotes have been plagued by them ever since, and alpha-proteobacteria still have them.

   There are many other species of prokaryotes from both the bacterial and archaeal domains, with group II elements too (and as I googled to make sure, there are even some with group I introns now discovered), besides alpha-proteobacteria.

   There are alternative hypotheses, such as the idea that the entire spliceosome we see in eukaryotes, is actually ancestral and was somehow lost over evolutionary time. As you note, that idea doesn’t make much sense, since you could just ask why it wasn’t lost even before that, and then you have to invent additional ad-hoc explanations. So the simplest, most parsimonious hypothesis is that the spliceosome wasn’t ancestral, but evolved in eukaryotes, gradually as an adaptation to the initial invasion of group II self-splicing introns horizontally transferred from the alpha-proteobacterial endosymbiont, to the archaeal host genome.

2. CharlieM: In a talk which is well worth listening to, according to John Mattick

   Nothing John Mattick says is worth listening to.

   The fact that some cases of functional introns have been found doesn’t mean all introns are functional. They aren’t. Stop listening to crackpots.

   Yes, John Mattick is a crackpot.

3. Rumraket:

   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.

   Do all or any of the other skeptics here agree with this?

4. CharlieM: 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.

   A phenomenon known as pervasive transcription, predicted from first principles of how DNA binding proteins work.

   In an experimental test of transcription using a random piece of DNA (a piece of DNA deliberately constructed to be a nonfunctional piece of crap), organismal transcription machinery pervasively transcribed it as if it was a piece of chromosome. It’s simply a byproduct of how transcription works.

   From Non-coding RNA: what is functional and what is junk?
   Alexander F. Palazzo* and Eliza S. Lee
   Front Genet. 2015; 6: 2. doi: 10.3389/fgene.2015.00002

   It is important to recognize that the pervasive transcription associated with the human genome is entirely consistent with our understanding of biochemistry. Although RNA polymerases prefer to start transcription at promoter regions, they do have a low probability of initiating transcription on any accessible DNA (Struhl, 2007; Tisseur et al., 2011). Indeed it has been observed that most nucleosome-free DNA is transcribed in vivo (Cheung et al., 2008) and that many random pieces of DNA can promote transcription by recruiting transcription factors [TFs; see figure S4 in White et al. (2013)].

5. Rumraket: Nothing John Mattick says is worth listening to.

   The fact that some cases of functional introns have been found doesn’t mean all introns are functional. They aren’t. Stop listening to crackpots.

   Yes, John Mattick is a crackpot.

   Not everyone agrees with you:

   More recently, he was awarded the Julian Wells Medal by the Lorne Genome Society in 2009 and the International Union of Biochemistry and Molecular Biology (IUBMB) Medal in 2011. He received the HUGO Chen Award for Distinguished Achievement in Genetic and Genomic Research in 2012, the same year he was appointed Executive Director of the Garvan Institute of Medical Research.[1][4]

   Mattick was appointed an Officer of the Order of Australia in 2001 for service to scientific research in the fields of molecular biology, genetics and biotechnology, particularly through the development and administration of research institutes and the Australian Genome Research Facility.[5]

   I suspect what you mean to say is, “I disagree with much that Mattick says”.

6. CharlieM,

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

   Do all or any of the other skeptics here agree with this?

   The Evolutionary Landscape of Alternative Splicing in Vertebrate Specieswww.sciencemag.org
   Science 21 December 2012:
   Vol. 338 no. 6114 pp. 1587-1593 DOI: 10.1126/science.1230612

7. CharlieM: Not everyone agrees with you:

   Well fuck me, I guess that alone basically settles the matter.

   I say one thing, others disagree. That’s it, it’s all up for grabs we can all believe what we want.

   I suspect what you mean to say is, “I disagree with much that Mattick says”.

   Well you can’t help but disagree with crackpots now can you? No amount of titles and awards is going to make the crackpot things he say, not be crackpot. Isaac Newton believed that one of the most important areas of investigation was to elucidate the exact proportions of the first Temple of Solomon, because they contained “sacred ancient wisdom” about humanity, history and our place in the cosmos. By all accounts a brilliant man, perhaps one of the smartest men in all of history. Yet also a crackpot in many areas.

8. Rumraket,

   Are you saying that the amount of transcription going on in the human genome did not come as a surprise to the establishment?

   Here is one of the hits from the first page when I googled “pervasive transcription”.

   Pervasive transcription of the eukaryotic genome: functional indices and conceptual implications

   …surprisingly, the vast majority of the eukaryotic genome is dynamically transcribed in one setting or another, mostly as non-protein-coding RNAs (ncRNAs). Estimates range from 70% in nematode worm to 85% in fruit fly and 93% in humans. It is also clear that much of the genome is transcribed on both strands, and that many protein-coding loci also express antisense RNAs [6]. Moreover, recent data shows that many human genes (two-thirds of those examined) contain previously unrecognized first exons (and associated promoters) located at huge distances (an average of 186 kb; median 85 kb) upstream of the currently annotated start sites that are expressed in a tissue-specific manner and often span neighbouring genes [7], with similar results in fruit fly [8, 9], as well as intergenic splicing and fusion of transcripts that may be derived from widely separated locations including different chromosomes [10–14], and various types of post-splicing processing to produce smaller/variant transcripts.

   It may be very difficult to determine how much of this is actually functional but it should be noted that transcribed RNA is not just a one-dimensional string of nucleotides. As Sal has frequently pointed out it is a complex three dimensional structure, four dimensional if you include the time element. And the time element should be included as it affects the rate of translation.

   Drosophila dhc7 gene containing a ≥3.6 Mb intron takes roughly three days to transcribe

9. Rumraket: Well fuck me, I guess that alone basically settles the matter.

   I say one thing, others disagree. That’s it, it’s all up for grabs we can all believe what we want.

   Well you can’t help but disagree with crackpots now can you? No amount of titles and awards is going to make the crackpot things he say, not be crackpot. Isaac Newton believed that one of the most important areas of investigation was to elucidate the exact proportions of the first Temple of Solomon, because they contained “sacred ancient wisdom” about humanity, history and our place in the cosmos. By all accounts a brilliant man, perhaps one of the smartest men in all of history. Yet also a crackpot in many areas.

   So you are saying that Newton was considered a crackpot in many areas but he wasn’t a crackpot when it came to physics. Likewise Mattick may be a crackpot in many areas but he is not a crackpot in molecular biology.

   Well maybe you are right but I don’t know the man, so all I have to go on is his views on molecular biology and they don’t sound like the views of a crackpot to me.

10. CharlieM: Rumraket,

    Are you saying that the amount of transcription going on in the human genome did not come as a surprise to the establishment?

    Here is one of the hits from the first page when I googled “pervasive transcription”.

    Pervasive transcription of the eukaryotic genome: functional indices and conceptual implications

    Of ourse it came as a surprise to John Mattick in 2009.

    L O L

11. CharlieM,

    Well maybe you are right but I don’t know the man, so all I have to go on is his views on molecular biology and they don’t sound like the views of a crackpot to me.

    So what to make of the many who disagree with him? The problem with arguments from authority – other authorities.

12. CharlieM,

    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!

    If it were like that, it would be like that. But it isn’t like that, so it isn’t. [The problem with arguments from analogy].

13. Allan Miller: The problem with arguments from authority – other authorities.

    So many theories. We should probably not teach them in public schools, because that will only teach the little buggers to question authorities.

14. Allan Miller:
    CharlieM,

    So what to make of the many who disagree with him? The problem with arguments from authority – other authorities.

    It depends on why they disagree with him and his argument depends on the evidence that supports it. It isn’t the messenger, it’s the message and how well supported it is.

15. By rumrat’s logic we can say that all evolutionists are crackpots and aren’t worth listening to. The only authority they have in biology is the authority to stifle dissent with threats of academic jeopardy to all those who dare try.

16. Rumraket: Of ourse it came as a surprise to John Mattick in 2009.

    L O L

    The paper was referring to studies of data gathered in 2002 and 2005, so no it did not come as a surprise to Mattick in 2009.

    And as he said in 2007:

    …it is now evident that the majority of all animal genomes is transcribed, apparently in a developmentally regulated manner, suggesting that these genomes largely encode RNA machines and that there may be a vast hidden layer of RNA regulatory transactions in the background.

    And according to Gane Ka-Shu Wong1, Douglas A. Passey1, and Jun Yu1 in 2001:

    Most of the human genome is transcribed. However, the contrary idea—that little of the human genome is transcribed—is embedded deep in the popular consciousness.

    And it can be seen from a critical review of Matticks work in 2010, Most “Dark Matter” Transcripts Are Associated With Known Genes, that resistance to the idea of pervasive transcription lasted well into the 2000s.

    We conclude that, while there are bona fide new intergenic transcripts, their number and abundance is generally low in comparison to known exons, and the genome is not as pervasively transcribed as previously reported.

17. I would say the following details about Prof. Mattick would suggest that he is not a crackpot.

    In 2006 he was awarded an ARC Federation Fellowship, followed by an NHMRC Australia Fellowship in 2010, and pioneered studies on the function of non-coding RNA. He was appointed Executive Director of the Garvan Institute of Medical Research in 2012.

    Prof Mattick’s principal research interest is in understanding the role of non-coding RNA in human development, brain function and disease. He was the first to posit that most of the human genome specifies an RNA-based regulatory system. He was a member of the international consortia that discovered the expression of large numbers of long noncoding RNAs (lncRNAs) from mammalian genomes. He discovered ultraconserved elements in the human genome, and was the first to show cell- and stage-specific differential expression and subcellular localization of lncRNAs, their association with chromatin and chromatin-modifying complexes, and their perturbation in cancer and neurological diseases. Prof Mattick also discovered nuclear tiny RNAs associated with transcription start sites and splice junctions, and other classes of small RNAs. He showed that nucleosomes are preferentially positioned at exons, and that alternatively spliced exons are associated with promoters, revealing the dynamic organization of the transcription splicing complex.

    And he doesn’t sound much like a crackpot in this short video about the work done at the Garvan Institute.

    If he is indeed a crackpot then I’d like to see some evidence, someone’s personal opinion should not be enough to convince anyone.

18. CharlieM: If he is indeed a crackpot then I’d like to see some evidence, someone’s personal opinion should not be enough to convince anyone.

    Exactly

19. Allan Miller:
    CharlieM,

    So what to make of the many who disagree with him? The problem with arguments from authority – other authorities.

    I don’t see that as a problem. It is just the way science should work. New data quite often throw light on which views are closer to the truth.

    Maybe you could provide some examples of the data which contradict Mattick.

20. Allan Miller:
    CharlieM,

    If it were like that, it would be like that. But it isn’t like that, so it isn’t. [The problem with arguments from analogy].

    Can you be more specific as to why you think my analogy doesn’t hold up?

21. Mung,

    Frankie,

    newton,

    🙂 🙂 🙂

22. The textbook Biochemistry by Mathews et al. has a chapter on eukaryotic genes and their expression and within that chapter a section on introns. There is no discussion at all of how introns evolved. They take a functional approach to introns, rather than assuming they serve no function, and even provide a design explanation for introns.

    …the function of introns is not yet wholly understood. It seems likely that they serve as loci for genetic recombination, allowing functional parts of proteins to be interchanged in evolution. Such loci also allow some eukaryotes to make variants of a protein from a single gene, by splicing different exons together. This alternative splicing … is a more efficient way to store information than having a whole gene for each variant of the protein.

    Oh, and they unabashedly use terms such as “codes for” and “message” and “information” without resorting to scare quotes.

23. CharlieM:
    Mung,

    Frankie,

    newton,

    🙂 🙂 🙂

    Don’t be too happy because it applies to you as well.

24. newton: Don’t be too happy because it applies to you as well.

    Knowing that it applies to me too does not change my level of happiness 🙂

25. CharlieM: Knowing that it applies to me too does not change my level of happiness 🙂

    Glad to oblige

26. Mung:
    Oh, and they unabashedly use terms such as “codes for” and “message” and “information” without resorting to scare quotes.

    That’s because they’re writing for an audience who won’t deliberately misinterpret those words in disingenuous attempts to push their religious beliefs.

27. Mattick, of course, is famous as the originator of the dog’s ass plot. That seems good enough evidence that he’s a crackpot.

28. Patrick: That’s because they’re writing for an audience who won’t deliberately misinterpret those words in disingenuous attempts to push their religious beliefs.

    As opposed to those who choose to redefine those words is disingenuous attempts to push atheism/ materialism/ evolutionism.

29. John Harshman:
    Mattick, of course, is famous as the originator of the dog’s ass plot. That seems good enough evidence that he’s a crackpot.

    Your link takes us to the blog of T. Ryan Gregory, where he criticises a bar chart from an article by John Mattick. (At least I presume it was from Mattick)

    One criticism he makes is that

    It certainly would be a challenge to justify ranking humans as more complex than dogs — I can not think of any way that one could defend such a position objectively

    Well there is this for a start:
    James Olds, U.S. National Science Foundation

    The brain is the most complex biological structure known to scientists. When researchers do figure out how it works, they will accomplish perhaps the greatest scientific achievement in recorded human history.

    and:
    Decoding ‘the Most Complex Object in the Universe’

    The human brain contains some 100 billion neurons, which together form a network of Internet-like complexity. Christof Koch, chief scientific officer of the Allen Institute for Brain Science, calls the brain “the most complex object in the known universe,” and he’s mapping its connections in hopes of discovering the origins of consciousness.

    If humans possess the most complex objects in the known universe and dogs do not then I would take this as evidence that we can be regarded as more complex than dogs.

    Gregory then says:

    The sloping of the bars within taxa suggests that this is meant to imply a relationship between genome size and complexity within groups as well, with the largest genomes (i.e., the most non-coding DNA) found in the most complex organisms. This would negate the goal of placing humans at the extreme, as our genome is average for a mammal and at the lower end of the vertebrate spectrum (some salamanders have 20x more DNA than humans). Indeed, the human datum would accurately be placed roughly below the dog’s ass in this figure if it included a proper sampling of diversity.(my bolding)

    Gregory does something here that the the chart does not show. Since when did percentage of non-coding DNA equate to absolute genome size of an organism? How could he have made such a simple error in interpreting this chart is beyond belief. If humans had a genome which was orders of magnitude larger than any other organism on the planet but 99 percent of it coded for proteins then we would be at the far left of the chart, even prokaryotes would be above us on the chart.

30. Rumraket:
    You replied to Blas

    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.

    I then asked.

    Do all or any of the other skeptics here agree with this?

    So far no one here has come forward to say that they agree, but when I followed John Harshman’s, link, it led me to someone who does agree with you:

    Larry Moran

    I don’t think alternative splicing is very significant. Most of what is referred to as “alternative splicing” is artifact or splicing errors.

    Here are some quotes regarding alternative splicing:

    Science Daiy links to this article on alternative splicing:

    Alternative splicing occurs for the vast majority — 90 to 95 percent — of human genes, belying the popular notion that one gene codes for just one protein. The process also occurs for a high percentage of genes in many other animals and even in many plants. Alternative splicing is considered a fundamental amplifier of functional diversity, without which organisms on our planet would be far less complex.

    And from the University of Toronto, Why We’re Smarter Than Chickens

    AS (alternative splicing) enables cells to make more than one protein from a single gene, so that the total number of different proteins in a cell greatly surpasses the number of available genes. A cell’s ability to regulate protein diversity at any given time reflects its ability to take on different roles in the body. Blencowe’s previous work showed that AS prevalence increases with vertebrate complexity. So although the genes that make bodies of vertebrates might be similar, the proteins they give rise to are far more diverse in animals such as mammals, than in birds and frogs…

    …As scientists continue to sift through countless molecular events occurring in our cells, they’ll keep finding clues as to how our bodies and minds came to be.

    “This is the tip of an iceberg in terms of the full repertoire of AS changes that likely have contributed major roles in driving evolutionary differences,” says Blencowe.

    So who thinks that Rumraket and Larry are right?

31. Mung,

    So many theories. We should probably not teach them in public schools, because that will only teach the little buggers to question authorities.

    Nah – we should teach critical thinking, not authority. Authority is a bit of a Creationist thing anyway. It’s “Dr” this and “Professor” that and “Nobel Laureate” the other when an argument is being imported in imagined support of the Creationist position, but not even plain old “Mr” for those who disagree.

32. Frankie,

    It depends on why they disagree with him and his argument depends on the evidence that supports it. It isn’t the messenger, it’s the message and how well supported it is.

    Well, exactly. So why should anyone give a fuck what X thinks?

33. CharlieM,

    I don’t see that as a problem. It is just the way science should work. New data quite often throw light on which views are closer to the truth.

    Maybe you could provide some examples of the data which contradict Mattick.

    Why on earth should I do that? You bring him up, quote some of his words then toddle off to do the gardening while I argue with him?

34. CharlieM,

    Can you be more specific as to why you think my analogy doesn’t hold up?

    Sure. The thing you are analogising is not like the thing you are analogising it to …

35. Mung,

    Oh, and they unabashedly use terms such as “codes for” and “message” and “information” without resorting to scare quotes.

    Yeah, loads of people do. I sometimes go through my own prose and take the scare quotes out, as I think it can look a bit “arch”. So bleeding what?

36. Allan Miller: So bleeding what?

    But when they refer to the “RNA world” they do put that in quotes. It really doesn’t take much to amuse me.

37. CharlieM: Since when did percentage of non-coding DNA equate to absolute genome size of an organism? How could he have made such a simple error in interpreting this chart is beyond belief. If humans had a genome which was orders of magnitude larger than any other organism on the planet but 99 percent of it coded for proteins then we would be at the far left of the chart, even prokaryotes would be above us on the chart.

    Technically you are right. But in practice the amount of space spent on protein-coding sequences doesn’t differ all that much among eukaryotes, and genome size is a pretty good proxy for percentage of non-coding DNA. So in practice Gregory is right. Did you imagine that salamanders have 20 times more protein-coding DNA than humans?

    So who thinks that Rumraket and Larry are right?

    Anyone who knows much about the subject. There’s a lot of alternative splicing but very little of it can be shown to be functional. Same with pervasive transcription. Just as all this, the dog’s-ass plot is another example of a spurious attempt to make humans special.

38. It is estimated that at least one hundred proteins are involved in RNA splicing, making this process comparable in complexity to protein synthesis and initiation of transcription.

    – Molecular Cell Biology. Lodish et al.

    And it all just happened, by accident, and without it we probably wouldn’t be here.

    Praise Magic!

39. Allan Miller:
    CharlieM,

    Why on earth should I do that? You bring him up, quote some of his words then toddle off to do the gardening while I argue with him?

    Well would you like to argue with me directly.

    I wrote previosly:
    Science Daily links to this article on alternative splicing:

    Alternative splicing occurs for the vast majority — 90 to 95 percent — of human genes, belying the popular notion that one gene codes for just one protein. The process also occurs for a high percentage of genes in many other animals and even in many plants. Alternative splicing is considered a fundamental amplifier of functional diversity, without which organisms on our planet would be far less complex.

    Do you agree with them that alternative splicing is important in the evolution of complexity? Or would you say that it’s not very significant?

    If you think the former then maybe we will have something to argue about.

40. John Harshman: Just as all this, the dog’s-ass plot is another example of a spurious attempt to make humans special.

    Yeah, who needs a spurious attempt when it is obvious that we are special. When other animals can classify life I will reconsider.

41. John Harshman: Technically you are right. But in practice the amount of space spent on protein-coding sequences doesn’t differ all that much among eukaryotes,

    And this agrees exactly with what Mattick says at the start of this video The hidden layer of RNA regulation in human development

    John Harshman
    and genome size is a pretty good proxy for percentage of non-coding DNA. So in practice Gregory is right. Did you imagine that salamanders have 20 times more protein-coding DNA than humans?

    They have more protein-coding DNA relative to the size of their genome. Here is a more detailed chart from the video linked to above:(see below)

    John Harshman
    Anyone who knows much about the subject. There’s a lot of alternative splicing but very little of it can be shown to be functional. Same with pervasive transcription. Just as all this, the dog’s-ass plot is another example of a spurious attempt to make humans special.

    I disagree. From Wikipedia:

    Notably, alternative splicing allows the human genome to direct the synthesis of many more proteins than would be expected from its 20,000 protein-coding genes.

    Alternative splicing occurs as a normal phenomenon in eukaryotes, where it greatly increases the biodiversity of proteins that can be encoded by the genome

    If you think that the chart is inaccurate, can you tell me in what way is it inaccurate?

    (The chart I inserted seems to have ended up in the wrong location)

42. CharlieM: (The chart I inserted seems to have ended up in the wrong location)

    Nah, that’s the way they always appear in a comment.

43. So continuing Larry’s challenge.

    Molecular Cell Biology by Lodish et al. has significantly more coverage of introns than the biochemistry book I covered earlier. But still little or nothing on intron evolution other then repeating the story about why natural selection might cause introns to be lost.

    …presumably there was selective pressure to lose nonfunctional DNA during the evolution of microorganisms.

    Group I introns are discussed, but not how they evolved. Group II introns are discussed, but not how they evolved.

    We learn that:

    RNA splicing is carried out by a very large ribonucleprotein complex, the spliceosome, that is assembled by interaction of five different snRNP particles with each other and with pre-mRNA. The spliceosome catalyzes two transesterification reactions that join the exons and remove the intron as a lariat structure, which is subsequently degraded.

    Group II self-splicing introns, which are found in chloroplast genes and mitochondrial genes of plants and fungi, exhibit a largely conserved secondary structure, which is necessary for self-splicing. The snRNAs in the spliceosome are thought to have an overall secondary structure similar to that of group II introns.

    The similaries in these structures suggests that the spliceosomal snRNAs evolved from group II introns, with the trans-acting snRNAs being functionally analagous to the corresponding domains in group II introns.

    An extension of this hypothesis is that introns in present-day nuclear pre-mRNAs evolved from ancient group II self-splicing introns through the progressive loss of internal RNA structures, which concurrently evolved into transacting snRNAs that perform the same functions.

    So there you have it, how introns evolved from, wait for it, other introns, by loss.

    While at the same time the spliceosome was born.

    I believe in miracles. Don’t you?

44. CharlieM: Do you agree with them that alternative splicing is important in the evolution of complexity?

    The evolution of snRNAs may have been an important step in the rapid evolution of higher eukaryotes. As internal intron sequences were lost and their functions in RNA splicing supplanted by trans-accting snRNAs, the remaining intron sequences would be free to diverge. This in turn likely facilitated the evolution of new genes through exon shuffling. It also permitted the increase in protein diversity that results from alternative RNA splicing and an additional level of gene control resulting from regulated RNA splicing.

    Molecualr Cell Biology. Lodish et al.

    So many design benefits!

45. CharlieM: And this agrees exactly with what Mattick says at the start of this video The hidden layer of RNA regulation in human development

    This was in response to my statement that “But in practice the amount of space spent on protein-coding sequences doesn’t differ all that much among eukaryotes”. You contradict yourself here, though I suppose you didn’t notice. If that space doesn’t differ, then genome size is a good proxy for percentage of non-protein-coding DNA. Which means that Gregory’s chart invalidates Mattick’s dog’s-ass plot.

    [Salamanders] have more protein-coding DNA relative to the size of their genome. Here is a more detailed chart from the video linked to above:(see below)

    That’s just a more elaborate dog’s-ass plot, and it has the same faults as the original. Further, it doesn’t include any salamanders and so is irrelevant to supporting your claim. You have also just contradicted your previous statement. No, salamanders do not have more protein-coding DNA relative to the size of their genomes; that would require them to have more than 20 times as much protein-coding DNA as humans.

    I disagree. From Wikipedia:

    Wikipedia is not always reliable. Do you have any actual support for the claim that most alternative splicings are functional?

    If you think that the chart is inaccurate, can you tell me in what way is it inaccurate?

    Yes. The data are cherry-picked to support a point, perhaps not intentionally. It contains only sequenced genomes, and it should not be surprising to know that genomes to be sequenced, at the time, were chosen because they were small. Other than the human genome, of course, picked because it was the human genome. Genomes at the upper end of the distribution do not appear. If the plot had a true representative sample of genomes, the supposed pattern would go away.

    Again, consider Gregory’s chart of genome sizes, in light of your agreement that quantity of protein-coding sequence doesn’t differ much among eukaryotes.

46. CharlieM,

    Do you agree with them that alternative splicing is important in the evolution of complexity? Or would you say that it’s not very significant?

    I think for some genes it is very important. I don’t think it is significant in every gene in which it occurs. I think most isoforms are ‘noise’.

    I will note one of my favourite things here though – according to many ID advocates, proteins are on isolated islands of function and the v^n sequence space relationship between monomer library and string length is a vital consideration. Yet here we have a system where you can slice proteins every which way to Sunday, skip shuffle or add lengthy sections, and create multiple functional isoforms that are light years apart in ‘protein space’, if one were to take a naive bit-comparison view.

    I like that contradiction. When I try and mention modular shuffling as an evolutionary mechanism, a counter to the naive ‘bitwise’ Hoyle-o-matic view, I get a blank look.

47. From http://www.genomesize.com/statistics.php

48. Plants seem to span an incredible range in genome sizes. What’s in a genome? The C-value enigma and the evolution of eukaryotic genome content.
    Elliott TA, Gregory TR.

    Abstract
    Some notable exceptions aside, eukaryotic genomes are distinguished from those of Bacteria and Archaea in a number of ways, including chromosome structure and number, repetitive DNA content, and the presence of introns in protein-coding regions. One of the most notable differences between eukaryotic and prokaryotic genomes is in size. Unlike their prokaryotic counterparts, eukaryotes exhibit enormous (more than 60,000-fold) variability in genome size which is not explained by differences in gene number. Genome size is known to correlate with cell size and division rate, and by extension with numerous organism-level traits such as metabolism, developmental rate or body size. Less well described are the relationships between genome size and other properties of the genome, such as gene content, transposable element content, base pair composition and related features. The rapid expansion of ‘complete’ genome sequencing projects has, for the first time, made it possible to examine these relationships across a wide range of eukaryotes in order to shed new light on the causes and correlates of genome size diversity. This study presents the results of phylogenetically informed comparisons of genome data for more than 500 species of eukaryotes. Several relationships are described between genome size and other genomic parameters, and some recommendations are presented for how these insights can be extended even more broadly in the future.

    Another key factor that sets eukaryotic genomes apart is their size. The genomes of Bacteria and Archaea are all diminutive, in the range of 140 kilobase pairs (kbp) to approximately 15 megabase pairs (Mbp), with most of this variability accounted for by differences in the number of protein-coding genes [3]. In eukaryotes, by contrast, haploid nuclear genome sizes (‘C-values’) range more than 60 000-fold, from 2.3 Mbp in the parasitic microsporidian Encephalitozoon intestinalis [4] to approximately 150 000 Mbp in the plant Paris japonica [5], with this enormous diversity bearing no relationship to any intuitive notions of organismal complexity. This is not a new observation. Perplexingly large differences in genome size among morphologically similar species and the occurrence of corpulent genomes in comparatively simple organisms was first noted in the late 1940s and early 1950s. Twenty years later, this remained sufficiently confusing to be dubbed the ‘C-value paradox’ [6].

49. Mung: The evolution of snRNAs may have been an important step in the rapid evolution of higher eukaryotes. As internal intron sequences were lost and their functions in RNA splicing supplanted by trans-accting snRNAs, the remaining intron sequences would be free to diverge. This in turn likely facilitated the evolution of new genes through exon shuffling. It also permitted the increase in protein diversity that results from alternative RNA splicing and an additional level of gene control resulting from regulated RNA splicing.

    Molecualr Cell Biology. Lodish et al.

    So many design benefits!

    We all know Wikipedia is unreliable but even if they are wrong about the composition of the spliceosome it surely can’t be too far out.

    Wikepedia on the spliceosome

    Spliceosomes are a major component of an integral step in eukaryotic precursor messenger RNA maturation. A mistake in even a single nucleotide can be devastating to the cell, and a reliable, repeatable method of RNA processing is necessary to ensure cell survival. The spliceosome is a large, protein-RNA complex that consists of five small nuclear RNAs (U1, U2, U4, U5, and U6) and over 150 proteins. The snRNAs, along with their associated proteins, form ribonucleoprotein complexes (snRNPs), which bind to specific sequences on the pre-mRNA substrate.[7] This intricate process results in two sequential transesterification reactions. These reactions will produce a free lariat intron and ligate two exons to form a mature mRNA.

    5 snRNAs and over 150 proteins, that is an impressive construction!

50. CharlieM,

    And just for the hell of it, there’s another one …