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UCSD biologists identify 548 genes in the fruit fly likely to play a role in human genetic diseases

Biologists at the University of California, San Diego have identified genes in the common fruit fly, Drosophila melanogaster, that appear to be counterparts of genes responsible for more than 700 different genetic diseases in humans.

Their discovery, detailed in the June issue of the journal Genome Research, provides medical geneticists with a powerful new tool to identify the many genes that may be responsible for a particular human genetic disease and to understand its underlying biochemical mechanisms so that effective treatments can be developed.

"Scientists have long known that humans share many similar genes with fruit flies," says Ethan Bier, a professor of biology at UCSD who headed the research. "The surprise is how deep these similarities really are. Basically, every category of human genetic disease is well represented with a counterpart in the fly."

The UCSD scientists screened the genes involved in 929 human genetic diseases in their database against the fruit-fly genes in the complete Drosophila genome, published last March in Science. Their comparison of the amino acid sequences identified 548 fruit-fly genes that are so similar to genes involved in 714 human genetic disorders that the similarity could have statistically occurred by chance only one time out of 10 billion.

"If the probability was less than one out of 10 billion, we considered it a hit," says Bier. "That means that the proteins these genes code for are so similar that all of them or part of them most likely came from an ancestral protein."

Knowing which genes in fruit flies are the ancestral counterparts to genes that cause genetic diseases in humans is important to medical researchers for a variety of reasons.

"The fly offers an ideal model system in which these genes can be studied," explains Lawrence T. Reiter, a UCSD researcher and t
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Contact: Kim McDonald
kimmcdonald@ucsd.edu
858 534-7572
University of California - San Diego
14-Jun-2001


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