Here's a quick note on an National Human Genome Research Institute discovery reported in Science - another gene story, but this one is animals and the knowledge will be translated to humans.
Researchers at the NHGRI have discovered that mammalian chromosomes have evolved by breaking at specific sites rather than randomly as long thought - and that many of the breakage hotspots are also involved in human cancer.
By aligning and comparing the mammals’ genetic material, or genomes, the team determined that chromosomes tend to break in the same places as species evolve, resulting in rearrangements of their DNA.
Chromosomal breakages, also referred to as translocations, are thought to be important in terms of evolution. In addition to their evolutionary implications, chromosomal translocations are known to contribute to the development or progression of many types of cancer.
Here is the part I am facinated with: Based on an analysis that included a computer-generated reconstruction of the genomes of long-extinct mammals, researchers found the rate of chromosomal evolution among mammals dramatically accelerated following the extinction of the dinosaurs about 65 million years ago.
Okay, so....
Says the NHGRI, "Before the sudden demise of dinosaurs and many other types of animals, which is thought to have resulted from a massive comet or asteroid striking Earth, mammals shared fairly similar body plans and also fairly similar genomes. Researchers speculate that the mass extinction opened new ecological niches for mammals, spurring their diversification and the emergence of new mammalian orders. This situation would have facilitated opportunities for the isolation of mammals into more distinct breeding groups, speeding the development of species-specific chromosomes."
“This study has revealed many hidden secrets on the nature and timing of genome evolution in mammals, and it demonstrates how the study of basic evolutionary processes can lead to new insights into the origin of human diseases,” says Harris A. Lewin, director of the Institute of Genomic Biology at the University of Illinois.
Monday, July 25, 2005
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