Wednesday, April 10, 2013

Evolution and Junk DNA in Chicago

I just signed up for the SMBE Conference in Chicago in July. There's lots of cool talks about evolution but, in the end, I decided I just couldn't miss the session on "Where did 'junk' go?" with Wojciech Makalowski as organizer. Here's the blurb ...
Late Susumu Ohno once said "So much junk DNA in our genome" and the phrase junk DNA was born. For a long time mainstream scientists avoided these parts of the genome. However, over the years the picture slowly started to appear suggesting that the junk DNA hides a genomic treasure. With the completion of the current ENCODE project, junk DNA effectively disappeared because there's no longer useless DNA in the genome. This symposium will discuss the current understanding of these not-so-long-ago obscure areas of the genome, with special attention to transposable elements' activities and their evolutionary consequences. The integral part of the symposium will be general discussion of Ohno’s idea and its place in today's biology.
I'm familiar with Makalowski's way of thinking—it resembles the opinions of many Intelligent Design Creationists even though Makalowski is not a creationist [see Junk DNA: Scientific American Gets It Wrong (again)]. Back in 2007 he said,
Although very catchy, the term "junk DNA" repelled mainstream researchers from studying noncoding genetic material for many years. After all, who would like to dig through genomic garbage?
We know who's been invited to talk.
  1. Josefa Gonzalez (Institut de Biologia Evolutiva, Barcelona, Spain)
    "Adaptation is the key concept in Evolutionary Biology. Understanding adaptation has important scientific and social implications since adaptation underlies processes such as the ability of species to survive in changing environments, resistance to antibiotics and cancer chemotherapies and host-pathogen interactions, among others.
    However, adaptation is to date a very poorly understood process largely because the current approaches to the study of adaptation are often exclusively based on a priori candidate genes or on searching for signals of selection at the DNA level giving us an incomplete and biased picture of the adaptive process.

    In our lab we aimed at understanding the molecular process of adaptation and its functional consequences. Towards this end, we study recent transposable element (TE)-induced adaptations in Drosophila melanogaster."
  2. Valer Gotea (National Human Genome Institute, Bethesda, USA)
    "... it is not surprising that TEs [transposable elements] have a significant influence on the genome organization and evolution. What once was called junk now is considered a treasure. Although much progress has been achieved in understanding of a role that TEs play in a host genome, we are still far from a full understanding of the delicate evolutionary interplay between a host genome and the invaders"
  3. Dan Graur (University of Houston, Houston, USA)
    "This absurd conclusion was reached through various means, chiefly (1) by employing the seldom used “causal role” definition of biological function and then applying it inconsistently to different biochemical properties, (2) by committing a logical fallacy known as “affirming the consequent,” (3) by failing to appreciate the crucial difference between “junk DNA” and “garbage DNA,” (4) by using analytical methods that yield biased errors and inflate estimates of functionality, (5) by favoring statistical sensitivity over specificity, and (6) by emphasizing statistical significance rather than the magnitude of the effect."
  4. Dixie Mager (University of British Columbia, Canada)
    "The fact that transposable elements (TEs) can influence host gene expression was first recognized more than 50 years ago. However, since that time, TEs have been widely regarded as harmful genetic parasites-selfish elements that are rarely co-opted by the genome to serve a beneficial role. Here, we survey recent findings that relate to TE impact on host genes and remind the reader that TEs, in contrast to other noncoding parts of the genome, are uniquely suited to gene regulatory functions. We review recent studies that demonstrate the role of TEs in establishing and rewiring gene regulatory networks and discuss the overall ubiquity of exaptation. We suggest that although individuals within a population can be harmed by the deleterious effects of new TE insertions, the presence of TE sequences in a genome is of overall benefit to the population."
  5. Masumi Nozawa (National Genetic Institute, Mishima, Japan)
    (I don't know anything about his work. Can anybody help?


19 comments :

  1. With you and Dan there, this is going to be... interesting.

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    1. Now I have to be there. And fool of me I was thinking of that thing about next next next next generation sequencing ...

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  2. Dixie Mager says: the overall ubiquity of exaptation.

    Does she know what "ubiquity" means?

    Wow, some scientists really feel a need to over, over, over-hype their results.

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  3. Larry, you're just going to attend not give a talk?

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  4. I'm starting to realize just how ridiculous the adaptationist obsession has become to some evolutionary biologists.
    I recently saw a talk by Richard Dawkins and Lawrence Krauss, and Dawkins was asked in the Q&A period (as so many times before) to give his thoughts on why evolution would produce something like homosexuality. And of course, while he could speculate a bit on the matter, all of the suggestions sounded... well, quite frankly, ridiculous to me.

    I'm going to stick my neck out here and say that at this stage, it's obvious there's no very strong or compelling adaptive hypothesis that can account for homosexual behavior(at least in humans). In all likelyhood, since there is a genetic component (as suggested by Dawkins in the same video by reference to twin studies), it seems to me it has to be at least to some extend a byproduct of recombination.

    Speaking a bit simplistic and metaphorical, it makes much more sense to me to postulate homosexuality is the result of the occasional "wrong filter for determining sexual partners" arising through recombination during fertilization, than any of all the outrageously ineffective and uncompelling appeals to obscure selective pressures people have invented to try and account for it "evolutionarily".

    Now an adaptationist might respond that, since it isn't adaptive, why hasn't it degraded almost completely after millions of generations? Why does it consistently pop up at approximately 10% in so many sexually reproducing animals? What keeps it from drifting away completely?
    Well, what keeps the grey color of brainmatter to drift away completely? Surely the color of greymatter isn't selected for? Only the ability of brains to think? So the grey color of brains is a byproduct of the color of the constituents of brains, which is maintained for other reasons.

    In the same way, for homosexual behavior, the answer must obviously(?) be that, whatever recombinatorial result ultimately yields homoxexual behavior, all the individual genes must in isolation be maintained through purifying selection, because each of them have their various adaptive reasons for not drifting out of function. And so, once in a while, these genes are combined in such a way that somebody ends up finding their own sex attractive.

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    1. @Rumraket
      How does suicide fit into this? How about depression? 20-30 mil Americans suffer from this disorder mainly due to what? What is the underlining cause? Anybody can guess?

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    2. @Rumraket

      Homosexuality is also not invariably an absolute. A level of heterosexual activity would be enough to keep 'homosexual genetics' (whatever the underlying cause) in the population without invoking adaptation.

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  5. I'll be at the AOU meeting in August. Try to leave something for me. And be sure to visit the Field Museum before they disassemble it for parts.

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  6. @Larry,

    Forgive me but I'm a bit puzzled. While I treat your blog partially as relaxation from my reality of "big business small science world" and partially as a learning experience with pretty good and respected scientists posting here, I'm in a dismay today due to this post. I don't get you Larry. I just don't. Please admit it to me; small little guy that you are going there as fun an joke. Here is my psychoanalysis:

    You are not that old; you make mistakes but we all do. But this post and your going to Chicago to face and confront this issue...It's a bit thick. You are very strong when it comes to your beliefs, which is fine with me, I'm not judging you or recommending Adderall ...Let evolution be in-tacked when you get ill Larry. I'm not going to use THE WORD, because I respect you as a human being and as a colleague. I hope you are able to do the same...

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    Replies
    1. I'm not going to use THE WORD

      Use the WORD. Oh, use it, use it.

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    2. With colleagues like that who needs enemies ?

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  7. "Masumi Nozawa (National Genetic Institute, Mishima, Japan)
    (I don't know anything about his work. Can anybody help?"

    Here's a representative critique of his work (from Yang and Dos Reis, 2011, http://mbe.oxfordjournals.org/content/28/3/1217.full ):

    "In a recent simulation study, Nozawa et al. (2009a; see also Suzuki 2008) claimed that the branch-site test produced excessive false positives. However, the false-positive rate found by those authors was only 0.23%, much lower than the significance level (5%) (Yang et al. 2009). In another simulation, Nozawa et al. (2009b) discovered that the P value for the branch-site test generated under the null hypothesis showed a U-shaped distribution, with a slight peak (7.3%) in the interval (0, 0.05) and a very high peak in (0.95, 1.00), very different from the uniform distribution they expected. The authors considered the result to indicate an “abnormal behavior” of the likelihood ratio test and attributed it to small sample sizes in their simulation.

    However, the expectation of a uniform distribution for the P value is incorrect, as discussed by Zhang et al. (2005, p. 2473)."

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  8. Here's a telling quote from Makalowski in 2003:

    "Although catchy, the term “junk DNA” for many years repelled mainstream researchers from studying noncoding DNA. Who, except a small number of genomic clochards, would like to dig through ge- nomic garbage? However, in science as in normal life, there are some clochards who, at the risk of being ridiculed, explore unpopular territories. Because of them, the view of junk DNA, especially repetitive elements, began to change in the early 1990s. Now, more and more biologists regard repetitive elements as a genomic treasure."

    In other words, only clochards study non-functional DNA, but once they prove it functional, we can all study it!

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  9. Scientific American managed to write about the junk controversy without using the term junk! IMO Friction over Function: Scientists Clash on the Meaning of ENCODE’s Genetic Data is just another attempt to rescue ENCODE's 80% statement. This time it is not about everything being "functional“ but rather if something is “necessarily important for human life”. John Stamatoyannopoulos concedes that "ENCODE's definition of functional does not have anything to do with why certain regions might be important or what exactly the regions are doing for human health". IMO this is really dishonest because by moving the goalposts this way he can silently keep the 80% statement while at the same time he is trying to invoke the impression that ENCODE never was in disagreement with established scientific knowledge.

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  10. Isn't this exactly the sort of stuff that ENCODErs and "I'm Not Really A Pan-Adaptationists" have been saying /doesn't/ really occur? Every time someone acuses ENCODE of claiming to have found all junk DNA to be functional, their response is 'oh, that's not what we're really saying, and no one would really get that impression', and yet, here's an entire symposia at a conference with just that assumption!

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