Junk DNA is like bigfoot. If a zoologist says something like “Hmmm… it would be cool to find bigfoot” all the other zoologists jump on him or her, drag the poor sap into the alleyway, toss on a blanket, and beat the scientist with rubber hoses until the movement stops. Same with junk DNA. If you mention that junk DNA may have a use or a role or something …. INTO THE ALLY WITH YOU!!!

The difference is, there is no bigfoot, but there may be some interesting stuff happening in the so called junk DNA.

Part of the problem is in what we call “junk.” If it does something, it isn’t junk. So, for instance, there are genes where a string of codons code for a string of amino acids. But in order for that to happen, other parts of the DNA have to be involved … parts that are not the codons coding for the amino acids that will become part of the protein. That is obiovusly not “junk” but back a few years before these bits of DNA were understood, that was “junk.” You cans see the problem.

All of which is a long run-up to a press report from Princeton talking about a possible role for junk DNA. I’ll let the Princeton press report team speak for themselves, and then I’ll enjoy reading your comments:

To comment on this post, please visit this open thread on my old blogs. The commenting system on this blog is currently broken. Sorry for the inconvenience.

Scientists have called it “junk DNA.” They have long been perplexed by these extensive strands of genetic material that dominate the genome but seem to lack specific functions. Why would nature force the genome to carry so much excess baggage?

Now researchers from Princeton University and Indiana University who have been studying the genome of a pond organism have found that junk DNA may not be so junky after all. They have discovered that DNA sequences from regions of what had been viewed as the “dispensable genome” are actually performing functions that are central for the organism. They have concluded that the genes spur an almost acrobatic rearrangement of the entire genome that is necessary for the organism to grow.

It all happens very quickly. Genes called transposons in the single-celled pond-dwelling organism Oxytricha produce cell proteins known as transposases. During development, the transposons appear to first influence hundreds of thousands of DNA pieces to regroup. Then, when no longer needed, the organism cleverly erases the transposases from its genetic material, paring its genome to a slim 5 percent of its original load.

“The transposons actually perform a central role for the cell,” said Laura Landweber, a professor of ecology and evolutionary biology at Princeton and an author of the study. “They stitch together the genes in working form.” The work appeared in the May 15 edition of Science.

In order to prove that the transposons have this reassembly function, the scientists disabled several thousand of these genes in some Oxytricha. The organisms with the altered DNA, they found, failed to develop properly.

Other authors from Princeton’s Department of Ecology and Evolutionary Biology include: postdoctoral fellows Mariusz Nowacki and Brian Higgins; 2006 alumna Genevieve Maquilan; and graduate student Estienne Swart. Former Princeton postdoctoral fellow Thomas Doak, now of Indiana University, also contributed to the study.

Landweber and other members of her team are researching the origin and evolution of genes and genome rearrangement, with particular focus on Oxytricha because it undergoes massive genome reorganization during development.

In her lab, Landweber studies the evolutionary origin of novel genetic systems such as Oxytricha’s. By combining molecular, evolutionary, theoretical and synthetic biology, Landweber and colleagues last year discovered an RNA (ribonucleic acid)-guided mechanism underlying its complex genome rearrangements.

“Last year, we found the instruction book for how to put this genome back together again — the instruction set comes in the form of RNA that is passed briefly from parent to offspring and these maternal RNAs provide templates for the rearrangement process,” Landweber said. “Now we’ve been studying the actual machinery involved in the process of cutting and splicing tremendous amounts of DNA. Transposons are very good at that.”

The term “junk DNA” was originally coined to refer to a region of DNA that contained no genetic information. Scientists are beginning to find, however, that much of this so-called junk plays important roles in the regulation of gene activity. No one yet knows how extensive that role may be.

Instead, scientists sometimes refer to these regions as “selfish DNA” if they make no specific contribution to the reproductive success of the host organism. Like a computer virus that copies itself ad nauseum, selfish DNA replicates and passes from parent to offspring for the sole benefit of the DNA itself. The present study suggests that some selfish DNA transposons can instead confer an important role to their hosts, thereby establishing themselves as long-term residents of the genome.

source

Comments

  1. #1 George
    May 26, 2009

    Don’t tell Larry Moran about this!

  2. #2 sevişme videoları
    May 26, 2009

    virtually all the risk of pertussis in the vaccine refusers came from being unvaccinated, and 11% of the pertussis cases in the total population can be attributed to vaccine refusal. Can someone explain this better to me? if only 11% of the pertussis cases were vaccine refusers… were 89% of the cases…vaccinated people? Unvaccinated but not refusers? Babies?

  3. #3 anon
    May 30, 2009

    Very cool research. If people like Larry Moran and T. Ryan Gregory lifted their heads from the semantic sand they seem to be wallowing in, they might realize that there is actually some pretty fascinating research going on with certain types of “junk DNA.” It is exciting science.

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