ENCODE, the media, and what we really know about the human genome


5 Responses to “ENCODE, the media, and what we really know about the human genome”

  1. Baldhead says:

    Reminds me of when they first started this stuff, reported they`d worked out about 1%, and somehow that turned into `We know what every bit of our genes does`

  2. vonbobo says:

    Not a cylon!

  3. Jonathan Badger says:

    This is a particularly annoying case because as the article says, it isn’t just the typical “journalists don’t get science and write silly things about it” — the whole “80% functional” number is actually what the scientists in the ENCODE project are pushing. Which annoys the rest of us in genomics because this is only true if you use their definition of “functional”, which basically boils down to being transcribed even if the cell does nothing with it. According to this logic, radio static is functional because radios receive it and make it into sound.

  4. kimax says:

    For a response to this, and more information about ENCODE in general, read Ewan Birney’s blog: http://genomeinformatician.blogspot.co.uk/

  5. Preston Sturges says:

    80%? Well there has always been the camp that believes that histones, other DNA binding proteins, and DNA modification controls the world, and that’s been around for 20 years or more.  You can probably measure that in bulk, probably long before large scale DNA sequencing became possible.  I think people started advancing this theory many years before there was any empirical evidence, and it had sort of a crackpot feel about it because other stuff moved ahead so rapidly.

    But when there is some important bit of gene regulation, a close look at histones and DNA modification usually reveals something interesting about DNA or DNA binding protein modification, and now it’s recognized as being important and an under-developed field   I’m not aware that anybody found something interesting by starting with a search for DNA binding sites, so as far as I know it never became an engine driving a host of discoveries.  

    Of course, maybe this represents a baseline data set that will allow genome wide association studies of methylation or DNA binding with specific diseases. In fact, many common but mysterious diseases are likely to turn out to be the result of broad changes in transcriptional regulation in the genes commonly associated with the disease, but which lack mutations.

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