Tuesday, October 09, 2012

An Honest Intelligent Design Proponent?

It's unusual to find a proponent of Intelligent Design Creationism who makes an honest attempt to evaluate scientific facts. Jonathan McLatchie (Jonathan M) seems to be one of those rare birds. I'm not going to refer to him as an IDiot.

Here's a bit from his latest post on Evolution News & Views (sic [Perspectives on ENCODE and Junk DNA].
The debate thus hinges on whether activity such as transcription, transcription factor association, and histone modification are signs of true function. My own view is that such activity is suggestive of functionality, but not proof. Therefore I would be cautious about claiming that these results show 80% of the genome to have function in the sense that we normally use that word.

On the other hand, the observation that the genome is buzzing with activity underscores what proponents of ID have been saying for years: not knowing what something does doesn't constitute evidence that it's doing nothing. Moreover, it wasn't long ago that Laurence Moran and PZ Myers were telling us that the genome is not even pervasively transcribed and that this amounted to evidence that the majority of our DNA is junk.
That's pretty good for someone who posts on a blog that also publishes stuff from Jonathan Wells and Casey Luskin. I wonder if they talk to each other?

On the other hand, it's not perfect. I've been arguing for years that there is good solid evidence that most of our genome is junk. I have never used the argument from ignorance that Jonathan attributes to me.

Also, I have never denied that the genome is pervasively transcribed. Instead, I have argued that pervasive transcription is something that one expects given what we know about DNA binding proteins and transcription. I've pointed out that the vast majority of our genome is transcribed very rarely—about one transcript per day in 100 cells—and this is consistent with accidental transcription. This is noise. The product is junk RNA and is has no function [Useful RNAs?] [Junk RNA] [Pervasive Transcription] [How to Frame a Null Hypothesis] [How to Evaluate Genome Level Transcription Papers ].

I discussed this thoroughly when I reviewed Jonathan Wells' book The Myth of Junk DNA [Junk & Jonathan: Part 6—Chapter 3]. Perhaps Jonathan McLatchie hasn't read my earlier posts?

Contrast McLatchie's post with that of Jonathan Wells [A Dishonest Intelligent Design Proponent?].


15 comments :

  1. Larry Moran writes,

    "I have never denied that the genome is pervasively transcribed."

    Hmm, my apologies if I misrepresented your position. That was my interpretation of what you wrote here for instance. http://sandwalk.blogspot.co.uk/2010/05/junk-rna-or-imaginary-rna.html

    "In other words, most of our genome is not transcribed in spite of what was said in earlier papers."

    "Van Bekel et al. show that using RNA-Seq they detect very little transcription from the regions between genes. On the other hand, using tiling arrays they detect much more transcription from these regions. They conclude that the tiling arrays are producing spurious results—possibly due to cross-hybridization or possibly due to detection of very low abundance transcripts. In other words, the conclusion that most of our genome is transcribed may be an artifact of the method."

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    1. From the very same article:

      "We thought that much of the genome could be transcribed at a very low level but this was mostly due to accidental transcription from spurious promoters. This low level of "accidental" transcription is perfectly consistent with what we know about RNA polymerase and DNA binding proteins..."

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    2. Yes, I saw that bit. He writes immediately before the section you quote: "Many of us dismissed the earlier results as transcriptional noise or "junk RNA."" But the title of his article is "Junk RNA or Imaginary RNA?" And I thought the point of his article was to suggest that the perceived pervasive transcription might actually just an artifact of the method used. Maybe I've misinterpreted him though.

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    3. @Jonathan Mclatchie

      If read word by word, Larry’s article might appear confusing, as he addresses two sets of experimental data; one showing that most of the genome undergoes ‘accidental transcription’ (or ‘pervasive transcription’), and the other one showing that the first set of experimental data might be an artifact.

      However, as the title ("Junk RNA or Imaginary RNA?") suggest, Larry makes it clear that, either way, the notion of ‘junk DNA’ (jDNA) stands.

      Unfortunately, Larry and the other jDNA gate-keepers have not done their homework, which for real scientists includes keeping up with the scientific literature. As I commented intensively at this and other sites, all jDNA is functional, and that was shown more than two decades ago.

      The problem is that now the jDNA gate-keepers are too deep into their ‘honest mistake’ and don’t know how to ‘save face’ for their oversight. So they are just dodging and confusing the issue, hopping that the problem will go away.

      I call it ‘honest mistake’ because jDNA gate-keepers are partially right, in the sense that, indeed, jDNA function is not sequence-based as implied in the ENCODE’s conclusion.

      BTW, Jonathan, have you had the chance to take a look at the model about the evolution of genome size and the protective function of ‘junk DNA’ against insertional mutagenesis, which I discussed at large here at Sandwalk? See, for example: http://sandwalk.blogspot.com/2012/10/reddit-we-are-encyclopedia-of-dna.html

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    4. @Claudia Bandea

      If you proved all jDNA was functional over two decades ago, why haven't even well known ID proponents cited your work everywhere?

      Just how did you prove this, may I ask? And more importantly, why do onions need 5 times more jDNA than we do? Why do some species of onion need up to 5 times more jDNA than other species of onion?

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    5. ... or why do we need more than a chimp?

      http://www.ncbi.nlm.nih.gov/pubmed/12618366

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    6. Jonathan McLatchie wrote,

      Hmm, my apologies if I misrepresented your position. That was my interpretation of what you wrote here for instance. http://sandwalk.blogspot.co.uk/2010/05/junk-rna-or-imaginary-rna.html

      I was discussing the results from my colleagues Ben Blencowe and Tim Hughes. Their results indicated that pervasive transcription wasn't as pervasive as the preliminary ENCODE results suggested.

      The difference is due to different techniques used in the analysis. The consensus now seems to be that with the best techniques available you can detect transcripts complimentary to about 80% of the genome as long as you analyze a very large number of different cells and tissues.

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    7. Rumraket says: If you proved all jDNA was functional over two decades ago, why haven't even well known ID proponents cited your work everywhere?

      Possibly, because the ID proponents were not aware of this work; now that they are, I hope they will consider taking a serious look at this model on the evolution of genome size and the function of jDNA.

      I also hope that other researchers and scientists, particularly those in medical and health fields would evaluate the model, as it opens the door for better understanding of one of the most devastating maladies: CANCER.

      Briefly, according to this model, jDNA, which has originated from the activity of transposable elements and endogenous viruses, has been used by their hosts as a defense mechanism against insertional mutagenesis, which in humans is “…just a fancy way of saying CANCER.” For additional comments on this model you can start with: http://sandwalk.blogspot.com/2012/09/ewan-birney-genomics-big-talker.html

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    8. Rumraket says: Just how did you prove this, may I ask? And more importantly, why do onions need 5 times more jDNA than we do? Why do some species of onion need up to 5 times more jDNA than other species of onion?

      You might want to read some the dozens of comments I posted here at Sandwalk, in which I elaborated on the evidence and arguments for this model on the evolution of genome size and the function of jDNA.

      You might also want to read the original paper and the recent series of 5 mini-essays I posted in Science at: http://comments.sciencemag.org/content/10.1126/science.337.6099.1159

      Regarding the famous ‘Onion Test,’ which is a great metaphor for the C-value paradox, to my knowledge, I have been one of its most vociferous proponents, both here at Sandwalk and other sites; see for example:
      http://blogs.discovermagazine.com/loom/2012/09/05/another-science-hurricane-a-massive-survey-of-the-genome/, and
      http://blogs.discovermagazine.com/notrocketscience/2012/09/05/encode-the-rough-guide-to-the-human-genome/

      As you can imagine, as someone who has intensely promoted the ‘Onion Test,’ I must have at least a reasonable answer to this inconvenient question, as it applies to my model.

      Although relatively straightforward, understanding this model is not so easy, particularly on top of preconceived ideas. To start understanding it, you might want to read about the Hummingbird Case: http://sandwalk.blogspot.com/2012/09/athena-andreadis-writes-for-sceintific.html

      It might be a good idea to evaluate side by side, preferably by someone ‘neutral ‘, the Hummingbird Case and the Onion Test (of course, if the Onion Test is still standing as a relevant point; the reason I’m say in this is because the Onion Test is particularly relevant for hypotheses that say that jDNA has various sequence-based functions, which is not the case of my model).

      Here is a quote from my comment entitled: *C-value paradox and ‘junk DNA’ enigma: case solved?*, which should answer your question about onions:

      “As argued in the original hypothesis (1) and in the comments I posted here, by serving as a defense mechanism against insertional mutagenesis, which in humans and many other multicellular species leads to cancer, all jDNA is functional. Expectedly, as an adaptive defense mechanism, the amount of protective DNA varies from one species to another based on the insertional mutagenesis activity and evolutionary constrains on genome size.

      1. Bandea CI. A protective function for noncoding, or secondary DNA. Med. Hypoth., 31:33-4. 1990.

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  2. Claudiu, here's another thought: are humans better protected against insertional mutagenesis than bats, with their low C-value? The longevity of bats is extraordinary. How often do they die of cancer?

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    1. Piotr Gasiorowski says: Claudiu, here's another thought: are humans better protected against insertional mutagenesis than bats, with their low C-value? The longevity of bats is extraordinary. How often do they die of cancer?

      I don’t know the rate of cancer in bats, but that might be a very good lead to investigate (BTW Piotr, are you sure that you work is in linguistics not in molecular and evolutionary biology?) Because of their relatively small genome, bats might be under constrains on genome size similar to Hummingbirds. See my response above to Rumraket about the Hummingbird Case.

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  3. I don’t know the rate of cancer in bats, but that might be a very good lead to investigate (BTW Piotr, are you sure that you work is in linguistics not in molecular and evolutionary biology?)

    LOL, evolutionary linguistics is not all that different. We even have junk replicators (and linguists who believe every little piece of language structure must be functional, so they don't accept the junk idea)

    Because of their relatively small genome, bats might be under constrains on genome size similar to Hummingbirds. See my response above to Rumraket about the Hummingbird Case.

    Yes, I'm aware of that explanation. I just thought that if you're right about the protective function of the bulk of junk DNA, you should expect this protection to be less effective in size-constrained genomes like those of bats (and birds, why not?). I mean having a smaller genome (smaller cells, more efficient metabolism), while advantageous for fliers, would expose them to the negative consequences (if any) of junk reduction. On the average, both bats and birds have long life spans, so the increased risk of cancer should have some observable effects.

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    1. @Piotr

      Your suggestion is an excellent lead of investigation. There are others, for example: transgenic mice carrying large quantities of DNA sequences homologous to infectious retroviruses such as murine leukemia viruses (MuLV) might be more resistant to cancer induced by experimental MuLV infections as compared to controls.

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  4. Jonathan Mclatchie I'll just say cool Picture :P

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