Baltimore, MD The human genome shares several peculiarities with the DNA of just about every other plant and animal. Our genetic blueprint contains numerous entities known as transposons, or "jumping genes," which have the ability to move from place to place on the chromosomes within a cell.
An astounding 50% of human DNA comprises both active transposon elements and the decaying remains of former transposons that were active thousands to millions of years ago before becoming damaged and immobile. If all of this mobile and formerly mobile DNA were not mysterious enough, every time a plant, animal or human cell prepares to divide, the chromosome regions richest in transposon-derived sequences, even elements long deceased, are among the last to duplicate. The reason for their delayed duplication, if there is one, has eluded biologists for more than 50 years.
New research led by Carnegie's Allan Spradling and published online this week by Proceedings of the National Academy of Sciences provides potential insight into both these enigmas.
The scientists used the fruit fly, Drosophila melanogaster, one of the premier "model" organisms for studying genome structure and gene function. They focused on one particular transposon, called the P element, which has an unsurpassed ability to move that has stimulated its widespread use by Drosophila researchers.
Remarkably, P elements have only been present in Drosophila melanogaster for about 80 years, at which time they were acquired from the genome of a distantly related fruit fly species by an unknown process. P elements remain highly "infective" today. Adding just one copy to the genome of one fly causes all the flies in a laboratory population with which it breeds to acquire 30 to 50 P elements within a few generations. The original goal of the Spradling team's research was not to understand how transposons spread or genomes evolve, but something much simpler: To l
|Contact: Allan Spradling |