302 thoughts on “Introns”

1. What is the most recent and the most plausible explanation for the rise and fall of introns?

   They are an artifact of the Intelligent Design of organisms. They were required for alternative splicing which is an intelligently designed mechanism for producing more than one protein from any given gene.

   That is the only plausible explanation for it

2. 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.

   Not if you simply reverse the sketch you made. Self-splicing introns can insert themselves ‘selfishly’. They don’t benefit the organism, they benefit themselves, in much the same way a computer virus spreads on its own account, by hiding. Yes, yes, I know computer viruses are designed; save your energy on that score.

   Unlike many transpososon-type elements, which can’t remove themselves, these introns are non-disruptive in genes provided they excise cleanly. Where they do excise cleanly, the opportunity exists for all sorts of crap to accumulate in the crevice so formed.

   The mistake is in thinking that everything in a genome must be adaptive for the organism. Of course once you have such boundaries, you have the means to shuffle and drop exons, which can be adaptive.

3. Frankie: They are an artifact of the Intelligent Design of organisms. They were required for alternative splicing which is an intelligently designed mechanism for producing more than one protein from any given gene.

   A mechanism? Thought ID didn’t do mechanisms.

4. Which of the two explanations will look like a just-so story to Mung? Frankie’s “artifact of the Intelligent Design” or Allan’s well articulated, highly descriptive one?

   Bets are open.

5. Mung: to paraphrase dazz, they are used to it by now

   huh?

6. I should mention about 25% of the human genome is intron; less than 2% is exon. So if you wanted alternate versions of the proteins, you’d need c12 times as many alternate versions per gene to make the extra space cost-effective, compared to actually using it to ‘code’. And those alternate versions could be specifically tuned, which is not available when the same exons need to be used in many different proteins.

7. dazz: huh?

   It’s not you, it’s him.

8. “It’s sooooo complex and I don’t understand it, therefore GAWDDIDIT!!”

   Do these IDiots ever offer anything different?

9. Links from The Nature Institute”

   “Several new studies indicate that rapidly cycling cells constrain gene-architecture toward short genes with a few introns, allowing efficient expression during short cell cycles. In contrast, longer genes with long introns exhibit delayed expression, which can serve as timing mechanisms for patterning processes [such as occur during embryonic development]. These findings indicate that cell cycle constraints drive the evolution of gene-architecture and shape the transcriptome of a given cell type” (Heyn, Kalinka, Tomancak and Neugebauer 2015, doi:10.1002/bies.201400138).

   Intron length affects timing of gene expression. Timing is very important during development. Does this demonstrate “selfish” intron behaviour?

   “Intron retention is overwhelmingly perceived as an aberrant splicing event with little or no functional consequence. However, recent work has now shown that intron retention is used to regulate a specific differentiation event within the haematopoietic system by coupling it to nonsense-mediated mRNA decay. Here, we highlight how intron retention and, more broadly, alternative splicing coupled to nonsense-mediated mRNA decay (AS-NMD) can be used to regulate gene expression and how this is deregulated in disease. We suggest that the importance of AS-NMD is not restricted to the haematopoietic system but that it plays a prominent role in other normal and aberrant biological settings” (Ge and Porse 2014).

   A regulatory role for introns. Accidents put to good use.

   “The conventional model for splicing involves excision of each intron in one piece; we demonstrate this inaccurately describes splicing in many human genes. First, after switching on transcription of SAMD4A, a gene with a 134 kb-long first intron, splicing joins the 3′ end of exon 1 to successive points within intron 1 well before the acceptor site at exon 2 is made. Second, genome-wide analysis shows that >60% of active genes yield products generated by such intermediate intron splicing. These products are present at ∼15% the levels of primary transcripts, are encoded by conserved sequences similar to those found at canonical acceptors, and marked by distinctive structural and epigenetic features. Finally, using targeted genome editing, we demonstrate that inhibiting the formation of these splicing intermediates affects efficient exon–exon splicing. These findings greatly expand the functional and regulatory complexity of the human transcriptome” (Kelly, Georgomanolis, Zirkel et al. 2015, doi:10.1093/nar/gkv386).

   Introns are not just paracitic insertions.

   Introns within the 5′ and 3′ untranslated regions have generally been ignored as functionally insignificant, if only because they couldn’t mediate the formation of different protein isoforms. But this is now changing, as other functions are being discovered. In fact, the very “presence of an intron and the act of its removal by the spliceosome can influence almost every step in gene expression from transcription and polyadenylation to mRNA export, localization, translation, and decay”. “All introns can influence gene expression regardless of their position relative to the coding region because they alter the protein makeup of the mRNA protein particle” and this in turn is involved in many aspects of gene expression regulation (Bicknell, Cenik, Chua et al. 2012).

   There are much more examples at the link I gave above.

   And what about exitrons?

   Exitrons (exonic introns) are produced through alternative splicing and have characteristics of both introns and exons, but are described as retained introns. Even though they are considered introns, which are typically cut out of pre mRNA sequences, there are significant problems that arise when exitrons are spliced out of these strands, with the most obvious result being altered protein structures and functions. They were first discovered in plants, but have recently been found in other metazoan species as well.

   The usual line when experts unearth more details of processes is, “it seems to be more complex than we thought”, I would like to ask, more complex than who thought?

10. Charlie M,

    Good stuff! A lot of that I had not seen before. Many thanks. God bless.

    Sal

11. Allan Miller: Self-splicing introns can insert themselves ‘selfishly’. They don’t benefit the organism, they benefit themselves

    So they know what they are doing and why? Really? What happens when they get inserted into a coding sequence? I bet it messes it up.

    these introns are non-disruptive in genes provided they excise cleanly.

    And they just know when it’s time to get out? Really?

12. Hi Sal

    I’m very happy to help. I knew this would be right up your street! 🙂

13. CharlieM:
    Hi Sal

    I’m very happy to help. I knew this would be right up your street!

    Dunning-Kruger Street

14. Frankie’s “artifact of the Intelligent Design” or Allan’s well articulated, highly descriptive one?

    Umm Allan never said that nor how blind and mindless processes didit. So Allan’s well articulated, highly descriptive explanation doesn’t refute ID nor does it support evolutionism.

    Introns splicing themselves in and then excising when the time is right- as if they know all of that. Evos will accept anything as long as they think it supports their position- even when it doesn’t. LoL!

15. Adapa:
    “It’s sooooo complex and I don’t understand it, therefore GAWDDIDIT!!”

    Do these IDiots ever offer anything different?

    Sometimes they say “common design.”

    Which explains everything that common descent does just by invoking it. The lack of “common design” (differences indicating divergence) that also matters to common descent is simply ignored.

    OK, not really different, but at least another complete failure to deal with the issues that in fact don’t support their claims.

    Glen Davidson

16. GlenDavidson,

    Of course you could discuss the research relevant to the thread or at least show that you are interested in it.

17. Glen:

    The lack of “common design” (differences indicating divergence) that also matters to common descent is simply ignored.

    God the Designer likes a little variety, except when he doesn’t. He also likes introns, except when he doesn’t.

18. GlenDavidson: Which explains everything that common descent does just by invoking it.

    Glen the equivocator strikes again! How are you defining common descent, Glen? I ask because when it isn’t in caps then all you are talking about is humans giving rise to humans- ie a typical family tree.

    The lack of “common design” (differences indicating divergence) that also matters to common descent is simply ignored.

    LoL! So a common design excludes divergence? Really?

19. keiths:
    Glen:

    God the Designer likes a little variety, except when he doesn’t.He also likes introns, except when he doesn’t.

    LoL! The blind watchmaker likes very little variety except when it doesn’t. It also likes introns, except when it doesn’t. Too bad the blind watchmaker can’t account for introns in the first place.

20. CharlieM:
    GlenDavidson,

    Of course you could discuss the research relevant to the thread or at least show that you are interested in it.

    Why? Did Mung explain anything, or just complain about evolution?

    Sorry, one needs to say something useful if one expects interest. You should try it.

    Glen Davidson

21. GlenDavidson: Did Frankie explain anything, or just complain about evolution?

    LoL! All Glen and the rest do is complain about ID and never explain anything in terms of blind and mindless processes

    Sorry, one needs to say something useful if one expects interest.

    And yet you and yours never do. Perhaps YOU should try it.

22. CharlieM:
    GlenDavidson,

    Of course you could discuss the research relevant to the thread or at least show that you are interested in it.

    That will never happen, Charlie. These guys aren’t interested in research and science. Dogma never is

23. Mung says,

    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.

    The Central Dogma of Molecular Biology is,

    The central dogma of molecular biology deals with the detailed residue-by-residue transfer of sequential information. It states that such information cannot be transferred from protein to either protein or nucleic acid. (F.H.C. Crick, 1970)

    I don’t see how inserting crap into a genome violates the Central Dogma. Perhaps Mung can explain ?

24. The function of spliceosomal eukaryotic introns is multi-purpose. We are discovering function after they are expressed, but they have important function before they are expressed as reconfigurable parking lots and highways for molecular machines like regulatory proteins.

    Much of the ncDNA before it is transcribed can be viewed as spacers and parking lots which also have epigenetic RAM in the form of histones (and occasionally DNA mehtylations). And how they function as a spacer or parking lot depends on the cell type, and there are at least 213 canonical cell types, but possibly thousands of cell types in actuality (skin cells, nerve cells, bone cells, sperm cells, etc.)

    So intron length is more than just about timing. It affects the way the Origami Code of higher order chromatin structure works between cell types to create configurations like the one below.

    Depicted below shows how DNA can serve as parking lots for molecular machines in gene expression. The location of the parking lots changes depending on cell type, and thus also the spacer locations. The spacer locations help isolate one transcription area from other transcription areas. These transcription areas go by names like Topologically Associated Domains (TADs) or transcription factories.

    Depicted below are molecular machines known as regulatory proteins parking on non-coding DNA. The complexity boggles the mind!

25. CharlieM,

    Hi Charlie
    Thanks for the info on introns. This helps the case for their function in the genome. Drosophila has a gene that takes 16 hours to express in development. This is due to the length of genes introns.

26. The previous diagram has a really groovy description on the STC blog:

    http://schaechter.asmblog.org/schaechter/2014/02/on-finding-jewels-in-the-junk.html

    Here are some more thoughts from the STC blog. They obviously put the complexity of eukaryotic spliceosomal introns in context:

    Now look at figure 2 from the top part. ‘Reading’ DNA (2 nm scale) has become sort of trivial today and includes a detailed understanding of sequence-dependent variations in DNA curvature and helix stability. Mapping nucleosomes—DNA wrapped around histone cores—has left far behind the initially simple DNase technique. Covalent modifications at the N-termini of histones—acetylation, methylation, phosphorylation—trigger the ‘tightness’ of DNA-wrapping around nucleosomes and the density of nucleosomes on a given DNA stretch (11 – 30 nm scale). The degree of compaction is actively controlled as a means to regulate promoter activity as is further compaction by so-called ‘scaffolding proteins’ (30 – 300 nm scale). Modifications on one histone—or the lack thereof—greatly influence which modifications will decorate neighboring histone subunits in a nucleosome: there is crosstalk. Also, a number of enzymes modify both histones and non-histone substrates e.g. proteins involved in transcription and even ribosomal proteins that interact with rRNA. Because of the emergent complex syntax it seems appropriate to exchange the iconic term ‘histone code’ for the term ‘histone language’. Last to mention here is the 30 – 300 nm scale where newly discovered long, non-coding RNA species, incRNAs, are involved in regulating the structure of chromatin together with a bunch of ‘scaffolding proteins’ as e.g. the SMC proteins.

    There was this stippled grey line tagged ‘spacer DNA’ in figure 1, a somewhat vague abbreviation. The DNA sequences of these ‘spacer’ DNA stretches are not important for the functionality of the promoter but their three-dimensional organization—including their histone-wrapping and higher-order structures—certainly is. They have to bring the enhancer elements in proximity to the promoter so that the enhancer-bound transcription factors can play their part of the tune. Axel Visel and his coworkers addressed this topic indirectly in a genetic approach asking to which extent distant-acting enhancers influence the looks of mice (craniofacial morphology) during embryogenesis.

    Take #3 – God Bless the Child

    The complexity the Intelligent Designer put in the eukaryotic animal cell boggles the mind.

27. Larry Moran: It states that such information cannot be transferred from protein to either protein or nucleic acid. (F.H.C. Crick, 1970)

    Prions transfer their spatial shape, ie information, to other proteins causing them to also change shape

28. Many of the parking lots in the picture here:

    Introns

    lie within the introns.

    Here is a description of the discovery some parking lots (aka ENHANCERs) lying within introns. These introns coordinate the configuration and movement of these “parking lots” (enhancers).

    http://www.pnas.org/content/106/47/19934.full

    The regulated expression of large human genes can depend on long-range interactions to establish appropriate three-dimensional structures across the locus. The cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encompasses 189 kb of genomic DNA, shows a complex pattern of expression with both spatial and temporal regulation. The flanking loci, ASZ1 and CTTNBP2, show very different tissue-specific expression. The mechanisms governing control of CFTR expression remain poorly understood, although they are known to involve intronic regulatory elements. Here, we show a complex looped structure of the CFTR locus in cells that express the gene, which is absent from cells in which the gene is inactive. By using chromatin conformation capture (3C) with a bait probe at the CFTR promoter, we demonstrate close interaction of this region with sequences in the middle of the gene about 100 kb from the promoter and with regions 3′ to the locus that are about 200 kb away. We show that these interacting regions correspond to prominent DNase I hypersensitive sites within the locus. Moreover, these sequences act cooperatively in reporter gene constructs and recruit proteins that modify chromatin structure. The model for CFTR gene expression that is revealed by our data provides a paradigm for other large genes with multiple regulatory elements lying within both introns and intergenic regions. We anticipate that these observations will enable original approaches to designing regulated transgenes for tissue-specific gene therapy protocols.

    Hopefully, those introns don’t look so junky now! They look like amazing robotic arms positioning molecular machines in just the right place to do the right job.

    The intron (and other ncDNA) positioning of molecular machines to make proteins reminds me of the man-made analogue of robotic arms positioning and operating tools in the making cars.

29. Frankie,

    So they know what they are doing and why? Really? What happens when they get inserted into a coding sequence? I bet it messes it up.

    Did you actually read what you responded to? You know what a self-splicing intron is?

30. Mung says,

    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.

    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.

    Mung asks,

    What is the most recent and the most plausible explanation for the rise and fall of introns?

    If you don’t know the answer then why not just ask for help instead of prefacing your question with your view that the answer is probably irrational? You don’t know the answer so don’t assume that nobody else does either.

    Allan Miller gave you the answer in comment #2. The first introns were undoubtedly group II self-splicing introns. Tom Cech got the Nobel Prize in 1989 for discovering them. The chemical reactions of self-splicing are the same as those of spliceosomal introns.

    Modern spliceosomal introns appear to have arisen from these original self-splicing introns through an intermediate stage where the group II intron acted in trans to assist removal of introns that had gradually lost the ability to self-splice.

    Protein factors that enhanced the efficiency of this reaction evolved and eventually the RNA acquired mutations making it dependent on those proteins for activity. At this point the primitive spliceosome became irreducibly complex.

    Over time the original group II intron evolved into the five small RNAs we see today in the spliceosome. Those five snRNAs still retain similarities to the original group II self-splicing intron revealing their origin. The hypothesis is known as “Five Easy Pieces.”

    All of this information, and much more, can be found with a little effort. Or you could just ask people who know about biochemistry and molecular biology. It’s never a good idea to assume you can challenge evolution just because of personal ignorance.

    Costa, M., Walbott, H., Monachello, D., Westhof, E., and Michel, F. (2016) Crystal structures of a group II intron lariat primed for reverse splicing. Science, 354:aaf9258. [doi: 10.1126/science.aaf9258]

    Doolittle, W. F. (2014). The trouble with (group II) introns. Proceedings of the National Academy of Sciences, 111:6536-6537. doi: [doi: 10.1073/pnas.1405174111]

    Lynch, M., and Richardson, A. O. (2002). The evolution of spliceosomal introns. Current opinion in genetics & development, 12:701-710. [doi: 10.1016/S0959-437X(02)00360-X]

    Martin, W., and Koonin, E. V. (2006). Introns and the origin of nucleus–cytosol compartmentalization. Nature, 440:41-45. [doi: 10.1038/nature04531]

    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]

    Roy, S. W., and Gilbert, W. (2006). The evolution of spliceosomal introns: patterns, puzzles and progress. Nature Reviews Genetics, 7:211-221. [doi: 10.1038/nrg1807]

    Sharp, P. A. (1991). ” Five easy pieces.” Science, 254:663-664.

    Will, C. L., and Lührmann, R. (2011). Spliceosome structure and function. Cold Spring Harbor perspectives in biology, 3:a003707. [doi: 10.1101/cshperspect.a003707]

31. stcordova,

    Ah Jeez, I can hardly be bothered any more. Reams and reams and reams of brain-dump, pretty pictures, it’s all rilly complex therefore ….

    You don’t have to post as if your eternal life depended on it, Sal. Discussion has become nigh impossible. You all think everything was designed. I think we got that.

32. While introns do not encode protein products, they are integral to gene expression regulation. Some introns themselves encode functional RNAs through further processing after splicing to generate noncoding RNA molecules. Alternative splicing is widely used to generate multiple proteins from a single gene. Furthermore, some introns play essential roles in a wide range of gene expression regulatory functions such as non-sense mediated decay and mRNA export.

    https://en.wikipedia.org/wiki/Intron

    The biological origins of introns are obscure.

    You don’t say.

    The book cited in the OP called them junk.

33. Allan Miller: You all think everything was designed

    When it’s pointed out that stuff is complex in opposite ways to which we could expect stuff to be complex they fall strangely silent. I think I see an OP coming up…

34. Larry Moran,

    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!

    This is from the op.

    Yet the argument you make is for the origin of spliceosome removed introns. What about the origin of group 2 introns?

35. stcordova: The complexity the Intelligent Designer put in the eukaryotic animal cell boggles the mind.

    The complexity the Intelligent Designer put in the simplest eukaryotic cell boggles the mind!

36. Regarding introns as spacers, it might be instructive to go back to an exchange between Jonathan Wells and Steve Matheson, Arthur Hunt and Larry Moran seven years ago (my how time flies!).

    http://www.evolutionnews.org/2010/06/the_factfree_science_of_mathes035521.html

    The Fact-Free “Science” of Matheson, Hunt and Moran: Ridicule Instead of Reason, Authority Instead of Evidence

    Of course, some introns involved in alternative splicing could be just inert spacers–as Sternberg acknowledged on June 3. But the 2010 Nature article cited by Sternberg also provided evidence that introns are “rich in splicing-factor recognition sites,” and the authors of that article predicted “regulatory elements that are deeper into introns than previously appreciated.”

    Nope nope nope. As we know now, these “spacers” may not be so inert after all, but more akin to information bearing robotic arms used to position proteins that service the genes. We are starting to realize this because introns also harbor HISTONES!

    As pointed out in the STC blog, alteration of these histones on ncDNA allows them the DNA/chromatin complex to be spatially manipulated. In combination with histone modification, proteins, RNA transcripts, these “spacers” are transformed into robotic arms that service the gene (as shown above).

    Now why the extra complexity for eukaryotes? Prokaryotes don’t go through so much trouble. But this is like asking why are Rube Goldberg machines complex when the task can be done more simply. The issue is, like the peacock’s tail, the extravagance of the Rube Goldberg machine seems to go beyond mere survival.

    Prior to Darwin’s time, extravagances in biology were seen as something that was put there in order to make observers wonder at the genius of the Rube Goldberg Machine Maker in the sky. In Darwin’s time, it was the peacock’s tail that was the symbol of extravagance. The peacock’s tail made Darwin sick. In the present day, we have so many more things that ought to make Darwin sick, like functional introns!

    One benefit of this extra complexity enables dynamically changing expression levels between cell types in multicellular animals. It would appear the Intelligent Designer had method in his madness. Praise be!

37. Allan Miller:

    Reams and reams and reams of brain-dump, pretty pictures, it’s all rilly complex therefore ….

    Therefore, at least in this case we’ve established how introns can be functional. There’s hardly been any discussion about the 3D aspect of introns as robotic arms for molecular machines.

    Sheesh, I’d think you’d be a little more appreciative of the new perspectives I’m offering. So much focus on transcription and just quoting snippets here and there without much mechanical insight.

    Now we know a lot more than we did in 2010 when the intron debate between Wells and Matheson, Hunt and Moran took place.

    Introns compose 30% of the genome or so. I don’t think it’s quite so easy to write them off today like Matheson did 7 years ago. One can see, given what I laid out above, it probably will be a lot harder to write them off after a few more decades of research.

    7 years is a long time to start setting the record straight on the old intron debate between Wells and Matheson, but better late than never.

38. stcordova: But this is like asking why are Rube Goldberg machines complex when the task can be done more simply.

    It’s because evolution cannot think about design in the same way designers like us can. You seem afraid to address this head on.

39. 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.

    I don’t think the origin of introns is impossible, I just find it miraculous. I mean, what are the odds? 🙂

    I’ll tell you what Larry, I’ll pull out some biochem and molbiol texts and see what they say about when, how, and why introns evolved. That’s a step in the right direction isn’t it? However, my experience has been that such books don’t cover evolution. They tend to stick to the facts.

40. stcordova: One benefit of this extra complexity enables dynamically changing expression levels between cell types in multicellular animals.

    Simplicity and elegance are strived for in design. Complexity can be implemented with simple, discrete components that are loosely coupled.

    You designer designs utterly unlike any human designer. And yet you use human designed artifacts as evidence for design in biology. Those robot arms, are they goldberg style contraptions? Is the software that runs them? No, and no.

    stcordova: Praise be!

    You are worshipping a process. The irony is strong.

41. stcordova: 7 years is a long time to start setting the record straight on the old intron debate between Wells and Matheson, but better late than never.

    It’s called science. We learn more, people change their opinions. What you are doing is not science, it’s some weird score settling combined with some sort of sense of resentment.

42. stcordova: The peacock’s tail made Darwin sick.

    Always worth checking the primary source when Sal is quoting.

43. stcordova,

    Introns can be functional. This does not make every base in every intron functional. This is exactly the same argument you’ve used on LINEs, SINEs, everything else. One functional sequence, and that’s 25% of the genome accounted for …

    I’m not going to get you to see this, and I am getting pretty bored saying it.

    Sheesh, I’d think you’d be a little more appreciative of the new perspectives I’m offering. So much focus on transcription and just quoting snippets here and there without much mechanical insight.

    These aren’t ‘new perspectives’. It’s just Google-copy-paste. I (and anyone else), am perfectly capable of going out and reading the literature (well, anyone except colewd, apparently!). The purpose of your posts, though, seems more to dazzle than to inform.

44. Allan Miller: Did you actually read what you responded to?

    Yes, you provided a caveat and that begs the question- you said:

    Unlike many transpososon-type elements, which can’t remove themselves, these introns are non-disruptive in genes provided they excise cleanly.

    And my response was- So they know what they are doing and why?

    Where they do excise cleanly, the opportunity exists for all sorts of crap to accumulate in the crevice so formed.

    That should create havoc for the gene involved.

    You know what a self-splicing intron is?

    Only what is written. But yes, self-splicing introns are just another biological feature that blind and mindless processes cannot account for.

45. Mung,

    It’s that pathetic detail thing again, isn’t it? Sequences, dates, organisms, inside leg. Now! Or I say …. Designed. Somehow.

46. Larry Moran: It’s never a good idea to assume you can challenge evolution just because of personal ignorance.

    It’s never stopped me before!

47. Mung: I don’t think the origin of introns is impossible, I just find it miraculous. I mean, what are the odds?

    You already sound like Sal. YEC is calling! You know you want it!

48. Allan Miller: It’s that pathetic detail thing again, isn’t it?

    Testable hypotheses. Else all you have is just another creation myth.

49. This is surreal- just because we can observe something, ie self-splicing introns, and it’s actions follow all of the rules of biochemistry that is not evidence that self-splicing introns arose via natural selection, drift or constructive neutral evolution. It is only evidence for their existence, what they can do and how they do it.

50. Allan Miller:
    Mung,

    It’s that pathetic detail thing again, isn’t it? Sequences, dates, organisms, inside leg. Now! Or I say …. Designed. Somehow.

    The irony- Somehow evolved by means of blind and mindless processes vs Designed. Somehow.

    Darwin set the standard evolutionists must meet. And there isn’t anything in any subsequent version that supersedes it.