Junky genomes, again


Also, Casey Luskin demonstrates his inability to comprehend a science paper, again. Creationists are obsessed with the idea that every nucleotide in the genome (and now the transcriptome) must have a function, an idea that is actively rejected by the available data, so Luskin reads a Nature paper on RNA and gets it completely backwards. Larry Moran has a quote from the paper that directly and plainly contradicts Luskin’s misinterpretation. Once again, we can all laugh at the inanity of the Discovery Institute.

Comments

  1. says

    Casey Luskin said: (emphasis mine)

    As an ID proponent, I’m still waiting for Darwinists to let go of their precious “junk” arguments for blind evolution and common descent and learn the lesson that you can’t assume that if we don’t yet see function for a biomolecule, then it’s probably just “junk.”

    Yes, and we’re all waiting for you to let go of your “junk arguments”! (but we’re not holding our breaths)

  2. bobxxxx says

    Once again, we can all laugh at the inanity of the Discovery Institute.

    Meanwhile the Disco idiots will continue laughing at their creationist customers all the way to the bank. How nice it must be for them to have no moral values at all so they’re able to make a living trying to destroy science education.

  3. Sven DiMIlo says

    *rolls eyes*
    Compare the genome sizes of Fugu, Homo, and Ambystoma and then argue that there’s no junk DNA. jeez!

  4. AK says

    From Larry Moran’s post:

    This is a point of view that creationists share with many scientists who haven’t studied the subject. They assume that the only reason for labeling most of our DNA junk is because we don’t know what it does. That’s just not true. There’s plenty of good evidence that most of our genome can’t be functional.

    This assumes we already know all the various modes of functionality. At a time shortly after the discovery of the genetic code, the functionality of enhancer and suppressor sequences was unknown, and those regions would have been dismissed as “junk”.

    As it happens, sheer length is probably enough to matter under some circumstances, when it comes between an enhancer and the promoter region or a suppressor sequence. It seems likely that a human polymorphism Scicurious recently wrote about (in Neurotopia) is an example:

    We know that there are two functional polymorphisms of the SERT. A functional polymorphism is a slight change in the DNA coding for your protein which will alter the way that protein is expressed or how functional it is. In this case, the two available for SERT are the long and short alleles which are actually on the promotor region for the SERT gene. It has been found that the short version of the allele will lead to less expression of the serotonin transporter in the brain.

    If length is the explanation, then the fact that accumulated point mutations have scrambled the ORF’s and created nonsense coding wouldn’t matter. Short insertions and deletions would constitute valid functional mutations.

    My own searches found some support for the idea that specific differences in the secondary or tertiary structure of DNA in the intervening regions may contribute to this difference. (I won’t post links because of the spam blocker, and anyway I’d have to go back and find them again.) If so, this would constitute another, very recently observed, mode of functionality. Personally, I suspect the researchers were speculating ahead of their evidence, but I didn’t finish reading what I found since it was tangential to what I was looking for at the time.

    I’m not trying to support ID or any other sort of creationism, but I’d strongly recommend not dismissing DNA with no known function as “junk” just because we don’t currently know of a function.

  5. says

    I’m not trying to support ID or any other sort of creationism, but I’d strongly recommend not dismissing DNA with no known function as “junk” just because we don’t currently know of a function.

    This is a very good point. It is entirely possible that all of our DNA does have a function, however minor. It seems difficult however to prove that a specific strand of DNA has no possible function. A “junk in the gaps” argument similar to the ‘God of the gaps” argument we see from religionists so often.

  6. says

    The really funny thing about ID creationists harping about discoveries of functionality in “junk” DNA or RNA, is that one of the primary ways that functionality is inferred is from using comparative studies to detect the effects of natural selection. A sequence that is found to be under selective pressures is probably doing something useful. The sorts of studies that Luskin cites are straight-up evolutionary biology. What’s he trying to argue for, again?

  7. Jadehawk says

    whether or not junk DNA has some hard-to-pin down function or not, it might well be a sort of vestigial organ of the genome. those organs sometimes have functions too, but they don’t seem to be important enough that having the organ cut out has any noticeable negative effects.

    forgive my ignorance, but has anyone ever done an experiment on those junk DNA strips, i.e. made critters with altered/chopped junk DNA strands? is it even possible to, for example, clone a set of mice and alter their Junk DNA to see if that would have any effects?

  8. says

    At a time shortly after the discovery of the genetic code, the functionality of enhancer and suppressor sequences was unknown, and those regions would have been dismissed as “junk”.

    Watson and Crick publish the structure of DNA: 1953. Jacob and Monod are publishing on beta-galactosidase regulation in E. coli: 1958. I’ve got a few papers from 1951 on regulation of gene expression lurking in my files somewhere. Exactly when are scientists supposed to have labeled regulatory elements “junk”?

  9. idlemind says

    Every base pair is sacred,
    Every base pair is great,
    If a base pair is wasted,
    God gets quite irate.

  10. amphiox says

    If choose to define “function” loosely enough, then everything has a function. For example:

    1. It takes up space, contributing to the total volume and mass of the organism in question, which is clearly vital to any critter’s survival.

    2. It makes the chromosome arms more symmetrical, and therefore more pleasing to the eyes of the molecular biologists who study mitosis. (For it is self-evident that the creator is fond of molecular biologists)

    3. It’s a decoy, a non-coding region of DNA where retroviral insertions and chance mutations won’t disrupt important genes.

    4. It slows down the rate of DNA replication, and therefore plays a small role in coordinating the sequence of cell division.

    5. It creates a subject matter that helps employ molecular biologists (yet more evidence that the creator loves molecular biologists)

  11. Kerlyssa says

    @#10
    If nothing else the junk dna serves as a placeholder, moving the ‘relevant’ portions of the dna by removing the ‘junk’ would have some pretty startling effects.

  12. Scott says

    As a non-biologist, I’m curious. Can we tell if any of the “junk” DNA is ever transcribed in any way? That is, is it ever read to generate proteins? Is the transcription process regulated well enough to only read the useful parts? Or is there some QA process that cleans up any useless RNA/proteins that do happen to get transcribed?

    Thanks.

  13. AK says

    @PZ Myers:

    AFAIK prokaryotes (both types) seldom use enhancers or suppressors, and beta-galactosidase regulation in E. coli isn’t one of the exceptions. I could be remembering wrong, however the process in E. coli and similar Prokaryotes is far less complex than in Eukaryotes. Basically, I’m assuming that any sequence(s) for which no known potential function exists is regarded as junk.

    I’ll use my one link for Gene Regulation in Eukaryotes, which by my very quick scan seems to be reasonably correct and complete (my own ultimate source is Lewin’s “Genes“), although they call suppressors “silencers” which IMO implies a digital effect when it’s really analog (although the best known examples are degenerate to the point of seeming digital). The linked site has its own link to a page describing “Bacterial” mechanisms (at the bottom).

    From the latter, describing transcription initiation in the lac operon:

    The binding site for RNA polymerase is called the promoter. In bacteria, two features of the promoter appear to be important:

    * a sequence of TATAAT (or something similar) centered 10 nucleotides upstream of the +1 site and

    * another sequence (TTGACA or something quite close to it) centered 35 nucleotides upstream.

    The exact DNA sequence between the two regions does not seem to be important.

    Each of the three enzymes synthesized in response to lactose is encoded by a separate gene. The three structural genes (so named because they encode a product) are arranged in tandem on the bacterial chromosome.

    I suspect even today many would describe “exact DNA sequence between the two regions” as “junk” since it doesn’t seem to matter, but in fact it carries information in its length, which means it isn’t junk, just uses a different data encoding scheme.

    Similarly, but much more so, for Eukaryotes.

  14. Tiina Järvi says

    Junk DNA = the material between certain people’s ears.

    (I love being mean…! *insert Cruella De Ville laugh here*)

  15. LtStorm says

    There’s probably something contradicting the idea, and even more likely just no basis for it, but;

    I’ve often wondered if there might be some sort of mechanism hidden amongst the junk that could discern “major” mutations that cause drastic changes in an organism (such as the rat-like progenitors of bats having the gene switched on that caused their fingers to grow long and spindly), and “intentionally” forcing another mutation on a gene relevant to the one causing that, as a sort of self-experimenting element in an organism’s DNA, to push forward major differentiations in organisms such as the formation of wings in bats, or the feathers for birds.

    Of course, I make no claims that this makes any sort of sense (dammit, man, I’m a chemist, not an evolutionary biologist!), but it’s something I’ve wondered about.

  16. amphiox says

    A lot of junk DNA it seems to me is the byproduct of the evolutionary mechanisms responsible for increasing genome complexity, ie gene duplications and lateral gene transfers such as retroviral insertions.

    When a gene duplicates the second copy becomes free to mutate without survival penalty because the first remains intact and functional, so the second copy can change and adopt new functions. But it is more likely that mutations in the second gene will destroy it, turning it into a pseudogene and junk DNA.

    Creationists always insist that mutation is solely a destructive mechanism that can’t generate new information. By insisting that all junk DNA actually has function, they are blowing their own prime argument out of the water. In fact, they are going several steps further that evolutionary biologists, because instead of just claiming that gene duplications can sometimes result in a second gene with altered new functions, they are trying to insist that ALL gene duplications have new functions!

    I wonder if Luskin realizes what a colossal strategic debating error he is making here. (Irrespective of the actual truth or non-truth of the argument itself)

  17. amphiox says

    How likely is it for a mutation in junk DNA to render it non-junk?

    For example, we know of many examples of mutations in a functioning gene shutting off its regulatory element or introducing a premature stop codon, turning the gene into a pseudogene.

    What about the reverse process? Could a point mutation create a new start codon in a stretch of previously silent junk DNA, or an insertion of a regulatory element result in transcription of a previously untranscribed region?

    The new protein that would be introduced into the cell’s metabolism would have some three dimensional shape and affinities for certain types of molecular interactions solely due to the laws of chemistry. In most cases it would probably simply get degraded by protein regulatory mechanisms, but if in some instances it escapes that fate, it might get itself incorporated into some biochemical pathway, maybe as an additional subunit in some complex, possibly at first only as a non-functional hanger-on, but with the accrual of further mutations, it could alter the function of that complex.

    Are there any known instances of such a sequence of events happening?

    I heard about a wasp species with a toxin that seems to have been derived from retroviral genes. Could something like this have happened in that case?

  18. Katkinkate says

    Posted by: amphiox @ 13 “If choose to define “function” loosely enough, then everything has a function. For example: … 3. It’s a decoy, a non-coding region of DNA where retroviral insertions and chance mutations won’t disrupt important genes. …”

    This point might have some validity. Has this been investigated?

  19. says

    “For example, we know of many examples of mutations in a functioning gene shutting off its regulatory element or introducing a premature stop codon, turning the gene into a pseudogene.

    What about the reverse process? Could a point mutation create a new start codon in a stretch of previously silent junk DNA, or an insertion of a regulatory element result in transcription of a previously untranscribed region?”

    Death and Resurrection of the Human IRGM Gene

    Cemalettin Bekpen1,2, Tomas Marques-Bonet1,3, Can Alkan1,2, Francesca Antonacci1, Maria Bruna Leogrande4, Mario Ventura4, Jeffrey M. Kidd1, Priscillia Siswara1, Jonathan C. Howard5, Evan E. Eichler1,2*

    1 Department of Genome Sciences, University of Washington, Seattle, Washington, United States of America, 2 Howard Hughes Medical Institute, Seattle, Washington, United States of America, 3 Institut de Biologia Evolutiva (UPF-CSIC), Barcelona, Spain, 4 Universita’ degli Studi di Bari, Bari, Italy, 5 Institute of Genetics, University of Cologne, Cologne, Germany
    Abstract

    Immunity-related GTPases (IRG) play an important role in defense against intracellular pathogens. One member of this gene family in humans, IRGM, has been recently implicated as a risk factor for Crohn’s disease. We analyzed the detailed structure of this gene family among primates and showed that most of the IRG gene cluster was deleted early in primate evolution, after the divergence of the anthropoids from prosimians ( about 50 million years ago). Comparative sequence analysis of New World and Old World monkey species shows that the single-copy IRGM gene became pseudogenized as a result of an Alu retrotransposition event in the anthropoid common ancestor that disrupted the open reading frame (ORF). We find that the ORF was reestablished as a part of a polymorphic stop codon in the common ancestor of humans and great apes. Expression analysis suggests that this change occurred in conjunction with the insertion of an endogenous retrovirus, which altered the transcription initiation, splicing, and expression profile of IRGM. These data argue that the gene became pseudogenized and was then resurrected through a series of complex structural events and suggest remarkable functional plasticity where alleles experience diverse evolutionary pressures over time. Such dynamism in structure and evolution may be critical for a gene family locked in an arms race with an ever-changing repertoire of intracellular parasites.
    Author Summary

    The IRG gene family plays an important role in defense against intracellular bacteria, and genome-wide association studies have implicated structural variants of the single-copy human IRGM locus as a risk factor for Crohn’s disease. We reconstruct the evolutionary history of this region among primates and show that the ancestral tandem gene family contracted to a single pseudogene within the ancestral lineage of apes and monkeys. Phylogenetic analyses support a model where the gene has been “dead” for at least 25 million years of human primate evolution but whose ORF became restored in all human and great ape lineages. We suggest that the rebirth or restoration of the gene coincided with the insertion of an endogenous retrovirus, which now serves as the functional promoter driving human gene expression. We suggest that either the gene is not functional in humans or this represents one of the first documented examples of gene death and rebirth.

  20. says

    I’m not trying to support ID or any other sort of creationism, but I’d strongly recommend not dismissing DNA with no known function as “junk” just because we don’t currently know of a function.

    I don’t see many scientists dismissing possible unknown functions. Do you? It’s the IDiots who really do commit a far worse fallacy: If a 25 bp sequence is found to have a new function, when previously it was thought to have none, it’s taken as proof that there’s absolutely no junk in the remaining zillion bps.

    The IDiots also seem to think that transcription automatically = function, but that’s another matter.

  21. Jadehawk says

    hmmm…. i wonder if simply having a neutral breeding-ground for new mutations is in-and-of-itself a selective advantage? I’d imagine a species with such a breeding-ground would always be full of random, unnecessary functions, which could help a handful of individuals survive a drastic change of environment. while on the other hand, a species with a smaller (or, for argument’s sake, no) such neutral section would have a larger percentage of its mutations in essential areas where even mutations that might later sometime become beneficial can be detrimental at the time of acquiring it, and therefore be selected against (thus, that species would then be missing that mutation at the time when it would have come in handy)

    am I making any sense?

  22. DLC says

    Well, if there is any unused or “Junk” DNA then it means God needed a rewrite ? a better editor ? had to redo things ?
    Ergo must be imperfect, ergo a lesser god, or (Gasp) non-existent! Or maybe just mysteriously created all that extra DNA just to mess with people’s heads. anybody seen a razor around here ?

  23. molliebatmit says

    Scott #16:

    As a non-biologist, I’m curious. Can we tell if any of the “junk” DNA is ever transcribed in any way? That is, is it ever read to generate proteins? Is the transcription process regulated well enough to only read the useful parts? Or is there some QA process that cleans up any useless RNA/proteins that do happen to get transcribed?

    We can tell if a sequence is transcribed — we can take the messenger RNA in a cell and reverse-transcribe it back to DNA, then sequence the DNAs that result.

    When that’s done, we see a large number of expressed mRNAs. Many can be mapped to a known open reading frame/gene/protein, although each gene in mammals tends to have many splice variants — the same genomic DNA sequence can result in many potential proteins as a result of mixing and matching pieces of coding sequence called exons.

    Although many expressed mRNAs can be matched to an open reading frame, others appear to lack start codons, and are therefore assumed not to be translated into protein.

    Does that make sense? I can clarify any of the terms, but I’m not sure with which terms you’re already familiar.

  24. amphiox says

    I believe it was Sean Carroll who called junk DNA “fossil DNA.” The specific sequence, distribution and pattern of it being a clear indication of the organism’s evolutionary history, and an unequivocal demonstration of common descent.

    Evolution predicts the existence of junk DNA and explains why it has the specific sequences it has, and its distribution in the genome, in every particular lineage.

    Creationism struggles to even explain why junk DNA is there.

  25. amphiox says

    #24:

    I don’t know if it has been investigated, but the decoy idea wouldn’t explain the sequence diversity we see in junk DNA. If you want some kind of genetic “sink” to absorb random mutations safely, you could make do with an endless repeat of a single base pair, for example. And if you were looking for a genomic defense against retroviral insertion, you’d expect selection of specific sequences capable for which viral reverse transcriptase would have higher affinity for than coding DNA sequences, and you’d expect to see those sequences preserved between lineages.

  26. amphiox says

    Yikes. I ask a question and the first reply is from Charlie Wagner????

    Was the question really that dumb?

  27. clinteas says

    Not my specialty,but isnt the last thing anyone including the dumb creationists should want is for all of the pseudogenes to have function,given that such a large number(8.5% or something I think,not counting those other mobile bits and pieces) of them are ERV’s?

  28. Honza says

    While reading the discussion, it occurred to me that perhaps you should check not only your biology books, but also yout dictionaries. Well, here it is:
    ———–
    Main Entry:junk
    2 a (1): old iron, glass, paper, or other waste that may be used again in some form (2): secondhand, worn, or discarded articles (3): clutter 1b b: something of poor quality : trash c: something of little meaning, worth, or significance
    ———–

    So, in conclusion Junk is something of LITTLE meaning, rather than NO meaning, as some of you try to argue.

  29. Matt says

    If you are at all religious, then categorically, you are ignorant of science and its facts which completely contradict the bible, koran, torah, talmud, etc…

    There is no compatibility between the truth of evolution and the myths that are religions.

    End of story. Either live in ignorance or wake up, join the 21st century, and get on with your life.

    …just needed to vent my spleen a bit. Ugh.

  30. Facilis, SP says

    If you are at all religious, then categorically, you are ignorant of science and its facts which completely contradict the bible, koran, torah, talmud, etc…

    That’s rather strong. Since these people are “ignorant of science” I saw you should stop getting treatments or taking medicine from the doctors who happen to be religious or accepting scientific reasearch from the 40% of scientists who are religious.
    Its stupid to just say one particular group is ignorant.

  31. says

    Creationists are obsessed with the idea that every nucleotide in the genome (and now the transcriptome) must have a function

    Of course not all of the genetic code is functional – some of it must be documentation!

  32. Matt says

    Facilis, it is not the science that is ignorant. It is the person. The science has been tested and proven. So I have no trouble getting a script from a religious physician, I just disagree with their superstitions. And if someone rejects evolution, that is ignorance.
    I’m not saying they are ignorant of how some science works (pharmacology, etc…), just that ultimately accepting myth over contradictory evidence exhibits willful ignorance.

    :)

  33. David Marjanović, OM says

    I’ve often wondered if there might be some sort of mechanism hidden amongst the junk that could discern “major” mutations that cause drastic changes in an organism (such as the rat-like progenitors of bats having the gene switched on that caused their fingers to grow long and spindly), and “intentionally” forcing another mutation on a gene relevant to the one causing that, as a sort of self-experimenting element in an organism’s DNA, to push forward major differentiations in organisms such as the formation of wings in bats, or the feathers for birds.

    Nope. There is no such thing as a major mutation! What turns normal fingers into bat fingers is just a slight overregulation of one gene. And feathers are just hollow protein spikes in the end — have you read the Tianyulong thread? Wing feathers are just the latest differentiation of feathers.

    (Also, the ancestors of bats weren’t rat-like but vaguely shrew-like.)

    What about the reverse process? Could a point mutation create a new start codon in a stretch of previously silent junk DNA, or an insertion of a regulatory element result in transcription of a previously untranscribed region?

    Has happened — the antifreeze proteins of icefish come from random junk. But of course this is extremely rare.

    “If choose to define “function” loosely enough, then everything has a function. For example: … 3. It’s a decoy, a non-coding region of DNA where retroviral insertions and chance mutations won’t disrupt important genes. …”

    This point might have some validity. Has this been investigated?

    I don’t think it has been, but wouldn’t it just create a reservoir for retroviruses & transposons, which is a distinctly unhealthy state of affairs?

    Wrong universe, Charlie.

    No, no — this time he’s (surprisingly) right. There’s no reason why freak accidents like this shouldn’t happen once in 50 million years.

    i wonder if simply having a neutral breeding-ground for new mutations is in-and-of-itself a selective advantage? I’d imagine a species with such a breeding-ground would always be full of random, unnecessary functions

    No. If you mutate a retroviral pseudogene, you still have a retroviral pseudogene.

    Also, the longer your genome, the more replicating you have to do, and the more mistakes (mutations) the polymerase will make…

    While reading the discussion, it occurred to me that perhaps you should check not only your biology books, but also yout dictionaries. Well, here it is:

    The argument from etymology is a logical fallacy. We’re talking about the meaning of junk DNA here, not that of junk.

    But if you want to introduce the term “trash DNA” for your 34,000 retroviral pseudogenes (…remember, you probably don’t have more than 18,500 functional genes, and if you do, they aren’t more than 25,000…), be my guest.

  34. AK says

    @David Marjanović, OM:

    There is no such thing as a major mutation! What turns normal fingers into bat fingers is just a slight overregulation of one gene. And feathers are just hollow protein spikes in the end — have you read the Tianyulong thread? Wing feathers are just the latest differentiation of feathers. [original emphasis]

    Absolutely false! That there’s “no such thing as a major mutation“. Homeotic mutations are exactly that. A single change to the coding section of a single protein can produce major changes all over the body, sometimes leading to an entire new bauplan.

    A good illustration is Homeotic Evolution in the Mammalia: Diversification of Therian Axial Seriation and the Morphogenetic Basis of Human Origins by Aaron G. Filler:

    Evolutionary change in the system of homeotic genes seems to be involved in body plan transformation. Modularity theory [22], [23] and a reexamination of mutationism in the light of modern morphogenetics [24], have opened the door to a major revision of evolutionary theory to accommodate this new understanding of body plan innovation.

    From the introduction.

    Skipping to the conclusion:

    Homeotic and dorso-ventral pattern change play a significant role in the generation of new body plans among the mammals. Clusters of morphogenetic changes in stem groups at the origin of the Ferungulata, the Metatheria, the hominiform hominoids, and other superordinal and ordinal groupings have been accompanied by sets of homeotic changes that result in new body plans. Evaluating a full array of homeotic changes rather than attending to simple counts of vertebral numbers makes this pattern evident.

    Also:

    These data also support the concept of a threshold effect in diversification of the mammals–progress awaited morphogenetic innovation. This supports an enlarged role for a mutational view [24] of evolutionary drive to update classic Darwinian and New Synthesis models of the past two centuries.

    I’d say by any objective standard Homeotic mutations would count as “major mutations”>

    22 Gould SJ (2002) The Structure of Evolutionary Theory. Cambridge, Mass.: Belknap Press of Harvard University Press.

    23 Schlosser G, Wagner GP (2004) Modularity in Development and Evolution. Chicago: University of Chicago Press.

    24 Stoltzfus A (2006) Mutationism and the dual causation of evolutionary change. Evol Dev 8: 304–317.