Tuesday, August 25, 2015

The apophenia of ENCODE or Pangloss looks at the human genome

This is a paper in French by Casane et al. (2015). Most of you won't be able to read it but the English abstract gives you the gist of the argument. I had to look up "apophenia": "Apophenia has come to imply a universal human tendency to seek patterns in random information, such as gambling."
In September 2012, a batch of more than 30 articles presenting the results of the ENCODE (Encyclopaedia of DNA Elements) project was released. Many of these articles appeared in Nature and Science, the two most prestigious interdisciplinary scientific journals. Since that time, hundreds of other articles dedicated to the further analyses of the Encode data have been published. The time of hundreds of scientists and hundreds of millions of dollars were not invested in vain since this project had led to an apparent paradigm shift: contrary to the classical view, 80% of the human genome is not junk DNA, but is functional. This hypothesis has been criticized by evolutionary biologists, sometimes eagerly, and detailed refutations have been published in specialized journals with impact factors far below those that published the main contribution of the Encode project to our understanding of genome architecture. In 2014, the Encode consortium released a new batch of articles that neither suggested that 80% of the genome is functional nor commented on the disappearance of their 2012 scientific breakthrough. Unfortunately, by that time many biologists had accepted the idea that 80% of the genome is functional, or at least, that this idea is a valid alternative to the long held evolutionary genetic view that it is not. In order to understand the dynamics of the genome, it is necessary to re-examine the basics of evolutionary genetics because, not only are they well established, they also will allow us to avoid the pitfall of a panglossian interpretation of Encode. Actually, the architecture of the genome and its dynamics are the product of trade-offs between various evolutionary forces, and many structural features are not related to functional properties. In other words, evolution does not produce the best of all worlds, not even the best of all possible worlds, but only one possible world.


Casane, D., Fumey, J., et Laurenti, P. (2015) L’apophénie d’ENCODE ou Pangloss examine le génome humain. Med. Sci. (Paris) 31: 680-686. [doi: 10.1051/medsci/20153106023]

73 comments :

  1. Most of you won't be able to read it
    And not just because it is in French. I'm at work with a very generous subscription policy and it's still behind a paywall for me. Given that French is dying as a scientific language, they might want to stave off the inevitable for a while by going open access.

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    1. Same here: institutional access to M/S via my university library account ends with vol. 22 (2006), with all more recent stuff paywalled away. But, perhaps still more strangely, the article is freely available, courtesy of the authors, via Researchgate. I have downloaded the PDF in case the journal demands it to be taken off.

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    2. There is a good reason for writing in French if the objective is to review the controversy for a Francophone audience.

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    3. Yes, Joe. Indeed, the author told me that the article is part of a series of handouts for his students. Although in theory they can all read English they're far more likely to read handouts that are in French.

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  2. In theory it's available through our library account, but they still want to be paid more than I feel inclined to pay. I've asked the lead author for a PDF file. We'll see if that works.

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  3. Knockouts in mice proved that much of so called junk DNA plays regulatory role in the development of important tissues in many different organs.
    Another problem is that by knocking out other parts of so called junk DNA leaves mice blind at night. The claim that mice are fine without much of the genome and therefore it must be junk is invalid because mice kept in the lab and not in natural surroundings don't need night vision without which they wouldn't survive.

    Same applies to human genome. Until knockout are done, evolutionists can claim anything they wish without any evidence but little by little their imaginary junk DNA is shrinking every day.

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    1. Megabase deletions in mice proved that they have vast amounts of junk-DNA.

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    2. Only a creationist can take devastating evidence, turn it around and present it as if it supports his ridiculous claims. Hilarious

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    3. How long were the mice evaluated after the megabase deletion?

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    4. 25 weeks.

      http://escholarship.org/uc/item/4fd0v6b0#page-4

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    5. Beau, that's a reasonable question. According to the abstract, "Viable mice homozygous for the deletions were generated and were indistinguishable from wild-type littermates with regard to morphology, reproductive fitness, growth, longevity and a variety of parameters assaying general homeostasis." Looks like they evaluated the mice long enough for them to mature and reproduce, and probably throughout their lives.

      (Ma et al. 2004. Megabase deletions of gene deserts result in viable mice. Nature 431: 988-993. I can't read the article without paying, so am basing this on the abstract.)

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    6. Lutesuite, sorry I didn't just wait for your reply. -- BLW

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    7. SM said:"Same applies to human genome. Until knockout are done, evolutionists can claim anything they wish ". So only a completely unethical experiment would convince you. Because the human junk DNA is different?

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    8. A pre-preint version of the Megabase knockout paper is here;

      http://escholarship.org/uc/item/4fd0v6b0

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    9. I'm going to be a contrarian. Knockout experiments actually provide limited evidence. If we look at a post-knockout mouse, and it seems to be OK, how small a difference in fitness could be we see? I'd say that a 1% lowering of fitness might not be detectable. The mouse would still look and act normal. Certainly 0.1% decrease of fitness would not be detectable.

      Conservation of stretches of DNA is much stronger evidence, since it would require far less natural selection. The lack of evidence for conserved sequences in a stretch of DNA gives us a strong presumption that variation there is neutral.

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    10. I agree with Joe that the megabase deletion experiment is not necessarily indicative of lack of function in those regions. In particular, more than a thousand sequences in the deleted region exhibit conservation between humans and miece. If those sequences are conserved, then they are likely under purifying selection; and if they are under purifying selection they probably are of functional relevance.

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    11. If we look at a post-knockout mouse, and it seems to be OK, how small a difference in fitness could be we see? I'd say that a 1% lowering of fitness might not be detectable. The mouse would still look and act normal. Certainly 0.1% decrease of fitness would not be detectable.

      This is obviously a crude and simplistic way of looking at it, but FWIW: How many genes would we expect to be included in the sections of DNA removed from the mice in this experiment if all of genome if functional? And how likely would it be for a mouse to remain viable if that many genes were simply missing?

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    12. The possibility that some conserved code is not necessary for survival or reproductions suggests that selection can be very subtle.

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    13. Another problem is that by knocking out other parts of so called junk DNA leaves mice blind at night.

      Citation? I am aware that the entire DNA component of mouse rod cells affects their light-gathering capacity; I am not aware that any knockout experiments have been done to investigate the DNA-complement requirement for this capacity to be retained.

      As an aside, specialisation of the entire genome to light-gathering in nocturnal eyes would tend to argue against any other bulk function in diurnal or eyeless organisms or in other tissues. Unless it's an unlikely kind of pleiotropy, where optical properties and 'something else' were simultaneously provided by the same excess bases. This isn't the victory for ID expectations that you think.

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    14. It's true that we could never tell if removal of megabases of DNA resulted in just a small decrease in fitness. However, it's also true that the results of the experiment show us that huge amounts of the mouse genome are not very important for survival.

      The result could have gone the other way.

      The idea that all or part of these megabases of DNA is actually functional in spite of the evidence to the contrary smacks of special pleading in the face of an undesired result. That's not to say that the argument is wrong—it certainly isn't—it's just that it isn't a very good argument.

      Conservation is a more difficult concept than most people realize. If you look at the human and chimp genomes, for example, there will be huge stretches that are >99% identical in sequence. This is not "conservation," it's just the fact that those sequences haven't had enough time to diverge.

      The longer species have diverged, the less "conservation" you see but even if species last shared a common ancestor tens of millions of years ago, there will still be stretches of very similar DNA at many loci. In order to say these are "conserved" you have to show that they have retained sequence identify in many different species, not just two.

      The "conserved" regions that we're talking about in these studies are not very big and not very well conserved. It's hard to know whether they are just accidental or whether they are under positive selection. To further complicate things, the actual loci aren't necessarily orthologous since it's impossible to align junk DNA sequences from distantly related species. That gives you lots of wiggle room to match up regions of accidental similarity.

      There are also complications due to the presence of similar defective transposons, viruses, and pseudogenes in these parts of the chromosome. Such sequences are non-functional but appear to be "conserved."

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    15. This is really interesting stuff because if I got it right, the portion of DNA for the knockout was picked based on the fact that part of it was conserved in humans, I take it that was to make the experiment as relevant to the human lineage as possible.
      But according to the paper this region was a "gene desert" which sounds to me like it was presumed to be non-functional for the most part.

      Am I missing something obvious here?

      How much time or generations are needed to consider a sequence conserved, hence under selective pressure to keep it?

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    16. lutesuite asks,

      How many genes would we expect to be included in the sections of DNA removed from the mice in this experiment if all of the genome is functional?

      People like John Mattick would say that the deleted regions have hundreds of genes for functional RNAs that play a role in regulating gene expression. The result of the experiment suggests that all of these hundreds of "genes" contribute less than 1% to the fitness of the individual mouse.

      The ENCODE Consortium would say that there are thousands of functional DNA sequences in the deleted segments. Most of them are responsible for binding transcription factors creating enhancers that are far removed from the genes they control. Again, the results suggest that if 80% of that DNA functional then all of it together makes only a marginal contribution to the fitness of a mouse.

      Some people may want to argue that a selection coefficient of less than 0.01 is still significant for hundreds of "genes" and thousands of enhancers combined but, as I said above, it looks an awful lot like a rather desperate attempt to deal with nasty little facts.

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    17. And Professor Moran's reply clarifies a lot, thanks

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    18. As regular readers here know, I have been promoting the idea that, although only a small percentage of the human genome has informational roles (iDNA), the rest of it is implicated in non-informational functions, such protection against insertion mutagenesis in both germ-line and somatic tissues (http://biorxiv.org/content/early/2013/11/18/000588).

      However, let's neglect this hypothesis and consider that most of the genome DNA in mice for example is indeed "junk DNA" (jDNA). Let's consider that deleting 10 or 20% of this putative jDNA in mice will have phenotypic consequences, such as smaller size or less vitality. How do we interpret these results? Is this jDNA functional?

      This is a type of experiment that Dan Graur and other researchers in the field of genomics are advocating as necessary to probe the functionally of the genomic sequences. However, as pointed out in the linked (and free) paper, this approach might be flawed.

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    19. I'm going to be a contrarian. Knockout experiments actually provide limited evidence.

      I'm a contrarian too. When knock-out mice were first available they were widely expected to make it easy to determine the function of any gene, but in practice many knock-outs had no visible phenotypic effects. People (like you, Joe, but not, I think, Larry) who took the analysis of Henrik Kacser and Jim Burns seriously, were not in the least surprised.

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    20. I'm quite familiar with the literature on knock-outs in mice (and yeast) since my lab used to work on those types of experiments. I was mildly surprised at the number of gene knock-outs that have no effect, especially in yeast.

      However, I was not the least bit surprised when the deletions of megabase pairs of junk DNA had no effect. Apparently the proponents of function weren't "surprised" either because they've come up with all kinds of rationalizations to explain why the deletion of huge amounts of "functional" DNA has no effect.

      I'm not denying that some of those rationalizations make a little bit of sense but it seems unlikely that deletion of hundreds of "genes" for regulatory RNAs and thousands of "functional" enhancers would have no obvious effect.

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    21. I was mildly surprised at the number of gene knock-outs that have no effect, especially in yeast.

      Doesn't it simply show that even functional DNA may have a much smaller effect on overall fitness than one would expect from studies of its functions, thanks to genetic redundancy and other compensatory mechanisms? (GULO comes to mind again: knocking it out causes little harm if vitamin C is available in the animal's diet). I wonder what the ID position is with regard to redundancy. Does God love or hate it?

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    22. Athel: "When knock-out mice were first available they were widely expected to make it easy to determine the function of any gene, but in practice many knock-outs had no visible phenotypic effects."

      Well, that was a poor rationalization. We would not expect, for example, that deleting many of the immune system genes would result in noticeable phenotypic effects.

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    23. I have a question for the experts please. It looks to me like the limit between functional and junk is not necessarily a discrete, hard limit. Please correct me if I'm talking out of my rear end, but if drift acts on "non functional" sequences, it seems reasonable to assume that ever so slightly beneficial traits might end up being removed and the sequence responsible for it altered by drift.

      Would an experiment like this be viable?
      Some bacteria that's able to produce enzymes to digest two different nutrients is exposed to different concentrations of both nutrients. One of them with very little concentration that might be tweaked so that producing the enzyme to digest it is just barely beneficial. I guess if there's a way to determine and model the fitness mathematically somehow, there would be a way to detect the lower limit for drift, bellow which, drift takes over and natural selection becomes irrelevant.

      Of course that wouldn't be a redefinition of functionality, but more of a way to determine an operational boundary between selection and drift and a way to compare the impact of both selection and drift on a controlled environment.

      This is probably a stupid idea by I guess I'll throw it out there anyway

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    24. "The chemical genomic portrait of yeast: uncovering a phenotype for all genes.

      Hillenmeyer ME1, Fung E, Wildenhain J, Pierce SE, Hoon S, Lee W, Proctor M, St Onge RP, Tyers M, Koller D, Altman RB, Davis RW, Nislow C, Giaever G.

      Genetics aims to understand the relation between genotype and phenotype. However, because complete deletion of most yeast genes ( approximately 80%) has no obvious phenotypic consequence in rich medium, it is difficult to study their functions. To uncover phenotypes for this nonessential fraction of the genome, we performed 1144 chemical genomic assays on the yeast whole-genome heterozygous and homozygous deletion collections and quantified the growth fitness of each deletion strain in the presence of chemical or environmental stress conditions. We found that 97% of gene deletions exhibited a measurable growth phenotype, suggesting that nearly all genes are essential for optimal growth in at least one condition."

      http://www.ncbi.nlm.nih.gov/pubmed/18420932

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    25. The chemical genomic portrait of yeast: uncovering a phenotype for all genes. Hillenmeyer ...

      Genetics aims to understand the relation between genotype and phenotype. However, because complete deletion of most yeast genes ( approximately 80%) has no obvious phenotypic consequence in rich medium, it is difficult to study their functions...


      And your point is?

      Have you missed the idea that the argument is about whether 80% of human DNA is functional, not about yeast. I don't know what the figure is for yeast, but I can accept that it might be 97%. So what? How does that affect the ENCODE estimate for humans? In case you are confused about it, I should point out that humans are not yeast.

      For serious readers I would also point out that the statement "complete deletion of most yeast genes (approximately 80%) has no obvious phenotypic consequence in rich medium" is badly phrased, and is only true if you add "one at a time" after "most yeast genes". If you delete 80% all at the same time you will certainly have some thoroughly dead yeast.

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    26. The yeast nuclear genome is tiny (about 12 million bp) and contains almost 6,000 protein-coding genes. For comparison, the nematode Caenorhabditis elegans has a genome eight times larger than that of yeast, with about 20,000 protein-coding genes (humans have a comparable number). The 6,000 yeast genes (96% of which don't contain even a single intron) make up about 70% of the total DNA sequence. We have to make allowance for a fair number, presumably hundreds, of RNA-producing genes. This means that well over 70% of the yeast genome can be expected to be functional in some way, and that there's very little junk there to begin with.

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  4. "the Encode consortium released a new batch of articles that neither suggested that 80% of the genome is functional nor commented on the disappearance of their 2012 scientific breakthrough.".
    . Anyone know what's meant by " the disappearance of their 2012 scientific breakthrough."?

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    1. Yes. It refers to the scientific breakthrough that 80% of the human genome (with gusts in the authors' comments up to 100%) is functional, and that they are no longer making that claim. Various excuses have been offered.

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  5. ENCODE is likely not going away even if much less than 80% is functional. Unless we know in advance exactly which sections have no functional role, from a medical standpoint it is folly to write off sections of DNA as having no possible role in health and disease. The 100% figure is a good working hypothesis until convincingly falsified. And how can it possibly be falsified since every possible contingency must be examined to do so and we've barely examined the space of trillions of transcriptomes in all sorts of developmental and special contexts.

    Better to assume the DNA might have a role than to be presumptuous like Dan Gruar. And even if Graur is right, can he actually identify the specific places in the genome where we will NEVER EVER find a role in health and disease? No. So he should just butt out because he adds nothing to the betterment of medical science.

    It's not just about transcription, but could be out-of-the-box applications. For example LINE-1 are part of optical systems in nocturnal mammals. Junk DNA could be used as a lens! No one saw that one coming.

    Non-coding DNA can also be a storage device for transient information outside of the DNA bases through cytosine methylation markings and indirectly through associated histone methylation, acetylation and deacetylation modifications. All this debate over spurious transcription misses other realms where DNA can play a role.

    The non-coding DNA can play a role as part of the substrate of epigenetic memory and who knows what else.

    The following paper points out the importance of the methylation marks in repetitive elements in cellular differentiation. This is quite a different issue than the debate over spurious transcription:
    http://www.sciencedirect.com/science/article/pii/S0888754311002400

    and repetitive elements are important for Polycomb protein interactions:
    http://www.researchgate.net/publication/232237065_A_repetitive_elements_perspective_in_Polycomb_epigenetics

    So it ain't all about transcription!

    Maybe ENCODE is backing away from the 80% transcription as evidence of function, but there are other evidences for function than just transcription (be it functional or spurious). I've just listed a few other evidences, and I expect that's only the tip of the iceberg.

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    1. The 100% figure is a good working hypothesis until convincingly falsified. And how can it possibly be falsified since every possible contingency must be examined to do so and we've barely examined the space of trillions of transcriptomes in all sorts of developmental and special contexts.

      So it isn't falsifiable at all? I see. Thanks for playing.

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    2. Haha, "you can't falsify it because I can make up an endless amount of ad-hoc rationalizations for function".

      You know that you actually have to have a hypothesis with a specific set of predictions for falsification to work, right LiarforJesus? If you don't have a hypothesis other than "all DNA is functional no matter what" then you don't even have a bona fide hypothesis, you just have unfalsifiable blather.

      Rationalizing the results of your findings after the fact so as to shield them from falsification isn't science, it's theology. And let's get real, you are here to do apologetics for Jesus.

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    3. For example LINE-1 are part of optical systems in nocturnal mammals. Junk DNA could be used as a lens!

      It's not any particular element in this case, it is the entire DNA complement of nuclei, and its orientation. You're mixing it up with your other current favourite, (some) active L1's in nerve tissue.

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    4. "other evidences for function than just transcription (be it functional or spurious). I've just listed a few other evidences"

      Evidences?

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    5. liarsfordarwin says,

      And even if Graur is right, can he actually identify the specific places in the genome where we will NEVER EVER find a role in health and disease? No. So he should just butt out because he adds nothing to the betterment of medical science.

      You do realize, don't you, that mutations in junk (non-functional) DNA can still have a effect on health and disease?

      To take just one example, there are mutations in nonfunctional intron sequences that create new splice sites leading to reduced expression of the protein encoded by the gene. This can cause genetic diseases even though the original DNA was junk.

      Just because a mutation of medical significance can be identified in a certain stretch of DNA does not mean that DNA has a function in healthy individuals.

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    6. ID creationists keep claiming junk DNA is a science stopper. But how many of them have actually got in a lab to find a function for something? All of the multiple experiments on junk DNA are always performed by "evilutionists".
      As usual, IDers can't grasp simple ideas like even if a certain amount of DNA can be known to be junk, that doesn't mean one can't look for function in some particular portion of DNA.

      It really takes a special kind of stupid to believe these scientists are science stoppers, the ones IDiots quote mine when scientists find something they claim they have no reason keep looking.

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    7. Dr. Moran,

      Thank you for your reply. Yes, I agree mutations in the junk DNA have an effect on health and diseases which is exactly ENCODE gets funding from the medical community. The fact non-coding DNA has influence on health and disease is a good enough operational definition of "function" as far as medical science is concerned.

      As far as your claim of spurious transcription, I could almost buy that if it were not for the CeRNA hypothesis:

      https://en.wikipedia.org/wiki/Competing_endogenous_RNA_(CeRNA)

      which pretty much says the soup of RNAs even from pseudo genes and other "junk" has a regulatory role.

      As far as the medical community is concerned, assuming 100% functionality and 100% role of junk DNA in health and disease is good enough working hypothesis for them to do their job. And their job is identifying regions of DNA involved in cancer, auto-immune diseases, diabetes, obesity, various heritable diseases, whatever.

      It's sort of counter-productive to do business otherwise unless we know in advance something definitely has no role in disease or health.

      Many times, as shown in GWAS studies, it takes a lot of knocking out and compromise of junk regions before effect becomes measurable, but surely there seems to be a role for those junk regions.

      I've agreed with you that ID never predicted junk DNA is functional in as much as some creationists argue for genetic deterioration. But that's a separate battle than going against fellow scientists in the ENCODE community who are researching the role of non-coding DNA in health and disease.

      If the CeRNA hypothesis is correct, your claim of spurious transcription is a spurious claim. It really is a little to early for either side to claim victory, but if the medical community like ENCODE data, I don't see a reason evolutionary biologists need to keep waging jihad against ENCODE.

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    8. The whole truth: Evidences?

      The plural is an interesting shibboleth: for some mysterious reason, anyone who uses it is almost certainly a creationist.

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    9. Sal Cordova insists in the stupid argument that junk DNA is a science stopper and even worse, he thinks that regulatory genes were thought to be junk as in junk = non coding DNA. Unbelievable

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    10. The whole truth: Evidences?

      The plural is an interesting shibboleth: for some mysterious reason, anyone who uses it is almost certainly a creationist.


      Not entirely, though:

      http://www.talkorigins.org/faqs/comdesc/evidences.html

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    11. Dazz, is it fair to say what was once thought to be junk dna, in some cases, had regulatory elements?

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    12. Lies reads: Just because a mutation of medical significance can be identified in a certain stretch of DNA does not mean that DNA has a function in healthy individuals.

      And Lies understands: Yes, I agree mutations in the junk DNA have an effect on health and diseases which is exactly ENCODE gets funding from the medical community. The fact non-coding DNA has influence on health and disease is a good enough operational definition of "function" as far as medical science is concerned.

      There is no hope for him.

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    13. Dazz, is it fair to say what was once thought to be junk dna, in some cases, had regulatory elements?

      If people thought it was junk, how did they find out it had regulatory functions?

      More importantly: Who found that out? Creationists?

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    14. I'm not a qualified opinion, but I'm in forums like this to try and learn something. And I'm pretty sure regulatory elements have been known to exist for a long time and are not a challenge to junk DNA.
      When scientists claim that x% of a genome DNA is most likely junk, they don't have a list of what exactly is non functional. There are good candidates for junk, and know genes with known functions, and known regulatory elements.

      That's why I argued it doesn't make sense to label junk DNA as a science stopper. You may find some function here and there, but the arguments for junk DNA remain valid. For all I know it's not like all of the functional (coding genes and regulatory elements) part is known, so if 90% of the DNA is thought to be junk based on genetic load or whatever and a full 1% of new function was found, it would still be a 90% junk, because not all the 10% that is functional is known.
      I hope some of the actual biologists chime in and provide informed insight

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    15. More importantly: Who found that out? Creationists?

      Lutesuite, that is of no importance at all. I don't reject or accept science on the basis of who made the discovery. I would like to think that you don't either.

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    16. Beau, it's important because some are claiming junk DNA is supposed to keep scientists from looking for function, which is manifestly false.

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    17. Thanks, Dazz. Get it now, Beau? Or do you need further explanation?

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    18. "As far as the medical community is concerned, assuming 100% functionality and 100% role of junk DNA in health and disease is good enough working hypothesis for them to do their job. And their job is identifying regions of DNA involved in cancer, auto-immune diseases, diabetes, obesity, various heritable diseases, whatever."

      The medical community doesn't have to assume functionality or non-functionality at all. If you're sifting through a pile of stuff and you find find a useful nail, it doesn't matter if that pile is junk or part of a multi-megabase operon. One's assumption either way is irrelevant. If you really need more nails, you'll keep sifting through the pile.

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    19. But if you know how to distinguish a nail from useless junk, it helps. Pretending everything is a nail is going to be decidedly unproductive.

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    20. Question is, why do creationists keep pretending the junk DNA thing is just an argument from ignorance? As in Just because you don't know what it does doesn't mean it doesn't do anything

      The only reason I can think of for people like Sal "liarsfordarwin" Cordova to defend the 100% function hypothesis should be the default one, is so they can go out and claim victory.

      Do they really expect this tactics to work? Do they really think scientists are going to ignore the evidence for junk DNA and buy that crap of the 100% function null hypothesis? I mean they usually target their religious zealots audience. This looks far too ambitious to me, LOL

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    21. Although evolutionary geneticists had had hints before, back about 1969 they were surprised that there was so much junk in the genome. (So much for the assertion that the wanted to see junk there). However at that time the evidence, or perhaps I should say the evidenceses, became very strong that much (not all) of the genome outside of the exons was junk.

      The unhappiness of creationists with this is purely an argument from Bad Design. They normally reject Bad Design arguments when their opponents make them, and say that one cannot guess the mind of the Creator (oops, I mean The Designer).

      But when junk DNA comes up, they make use of their own guess as to the state of mind of The Designer.

      Go figure.

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    22. "But if you know how to distinguish a nail from useless junk, it helps. Pretending everything is a nail is going to be decidedly unproductive."

      lutesuite,

      It doesn't matter. GWAS that liars is talking about above does not consider whether or not DNA is functional. It isn't part of the rationale of GWAS, and it certainly has nothing to do with the mathematics behind it. liar's argument is a straw man. He wants people to believe that if we think 90+% of the genome is junk, we'll just stop looking into genetic effects on medical diseases. So we should all believe the genome is mostly functional despite mountains of evidence to the contrary. It's ridiculous when you really consider the point he is trying to make.

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    23. Joe, as usual, is right about the history of junk DNA. Scientists were pretty resistant at first to the idea that a lot of the genome is junk. liar's bad null hypothesis that it is all functional is actually what most people thought at one time, until we learned more about what makes up the genome. We didn't just decide for some arbitrary reason that it was mostly junk; the weight of the evidence led to that consensus, long before creationists ever heard of junk DNA.

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  6. Didier Casane sent me a copy, and I have now read it. It is an excellent article that I recommend to anyone who can read French. As they're enthusiastic readers of Dan Graur's blog it won't surprise anyone that they are very much in agreement with him (and with Larry, of course).

    In almost their last sentence, they say "the French universities appoint few teacher-researchers (or none at all!) with a solid foundation of evolutionary biology." Not just French universities, unfortunately.

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    1. I read it this morning and enjoyed it greatly -- the science alongside the style and the authors' sense of humour.

      Another article by Casane and Laurenti that can be recommended to anyone with an interest in evolution, is the one on why coelacanths aren't living fossils (Larry quoted it on Sandwalk some time ago). It's open access, and also admirably written.

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    2. @Athel and Piotr,

      Perhaps one of you can 'drop' the article in Dropbox or another similar online repository?

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    3. Like John said.

      But if you prefer a Dropbox link, see here

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  7. Perhaps one of you can 'drop' the article in Dropbox or another similar online repository?

    Piotr has already done this, but I want to add that Dropbox no longer works on this computer, since they ended support for the operating system that I'm using (Mac OS 10.4.11). I've never upgraded because more recent versions of the operating system don't support "Classic" applications.

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    1. Those damn apples always screwing humanity, SMH :p

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    2. Well yes, Apple does sometimes get things wrong, especially since Steve Jobs died. But on this computer (bought in 2005) I can run software that I bought in Toronto in 1989, and it still does what it's supposed to do. Can anyone running Windows make a similar claim? Pages (which I don't much like and only use when someone sends me a .doc file that I need to edit) can open many old Word files that Word can't open.

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    3. Athel, I wasn't taking a cheap shot at Apple, sorry if that's how I came off. So just to clarify, in case of doubt, as a null hypothesis, I'm poking fun at the bible by default.

      I think Apple has the success they deserve. I may not like some of their strategies but Macs and IPhones are great devices IMO

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    4. I wasn't taking a cheap shot at Apple,

      No problem. Despite the lower-case a I misinterpreted your "apples". Anyway, none of us (I suppose) want a Mac vs. Windows war on this site, so consider my comment unwritten.

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    5. Can anyone running Windows make a similar claim?

      Yes, of course. I'm running Windows 8 and a number of programs that I obtained in the 1980s and 1990s.

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    6. Athel, it is not insuperably difficult to run two different versions of OS X on the same computer, if you don't want to purchase a newer one. (On the other hand, I don't know how recent a version of OS X your current machine will support.)

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  8. DOS programs still run on Windows 10, unless they depended on special hardware. MS Word has translators available that will open not only old Word documents, but also old WordPerfect documents.

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