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Research reveals "junk" DNA may function in DNA repair

05/13/2002 04:07 PM
A team of scientists from LSU and the University of Michigan Medical School have reported a new potential biological role for what has been called "junk" DNA.                    

Repetitive elements, or "junk" DNA, constitute more than a third of the human genome. Among these repetitive elements there are nearly two million transposable elements or retrotransposons. Until now, scientists only conjectured what these mobile elements did, if anything, within the genome.

In a paper published online May 13th in the journal Nature Genetics, the authors present data that demonstrates that these "jumping genes" may act as a DNA repair mechanism in mammalian cells.   

"Jumping genes" are not really normal genes but DNA segments, said Mark Batzer, professor of biological sciences at LSU and one of the lead researchers on the team. These pieces of DNA jump around in the genome, much like a virus, but without the ability to leave the cell. They produce duplicates of themselves that jump into other locations throughout the genome in a copy-and-paste process.      

The genome often suffers from double-stranded breaks because of stress, chemical contamination or other cellular insults. Cells can die as a result of double-stranded DNA breaks. Retrotransposons move throughout the genome looking for a double-stranded break, and when they find one they insert themselves between the ends, knitting that region of the genome back together.

In other instances the retrotransposons cut the genome themselves and jump into the break rather than installing themselves as part of a cellular DNA repair process. Most of the time these new insertions do not have a significant impact on the genome, Batzer said. But sometimes they can cause problems. A number of diseases such as haemophilia A and muscular dystrophy can be attributed to retrotransposon insertion activity within the genome.

"This work is extremely important because it gives us a glimpse into the potential function of a large part of the genome, which was previously unknown," Batzer said.

The team of researchers approached the problem from two complementary directions. Scientists at the University of Michigan Medical School led by John Moran used a cell culture system to directly observe the mobile elements' movements, while Batzer and his graduate students Jeremy Myers and Bethaney Vincent used a computational analysis of the draft sequence of the human genome in LSU's Biological Computation and Visualization Center to determine the magnitude of the process. The center played an indispensable part in the research, Batzer said. 

"This is a true tribute to the Louisiana Board of Regents' and the state's Information Technology Initiative," he said. "Because of it we're in the forefront of computational biology." 

The Information Technology Initiative is also funding LSU's purchase of a Beowulf computer cluster, which is expected to be one of the fastest parallel computing clusters in the world owned by a single university. Batzer said the cluster will help him tremendously in the hundreds of thousands of computations he has to make for his work.

Ronald Brown

LSU Media Relations

225-578-3867


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