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Washington—A team of scientists has decoded virtually the entire genome of the fruit fly, Drosophila melanogaster, a creature that for nearly a century has been at the center of studies to reveal the role of genes in disease, behavior, and development.
The feat not only will help scientists glean information about human biology and disease from genetic counterparts in Drosophila's genome but also appears to validate a controversial technique that is currently being used by some laboratories to sequence the human genome.
The milestone, announced here at the annual meeting of the American Association for the Advancement of Science, was achieved through a collaborative effort between researchers from a biotechnology company, Celera Genomics in Rockville, Md, and federally funded researchers, primarily the Drosophila Genome Project Group at the University of California, Berkeley. The team has identified more than 97% of the fruit fly's genetic code and virtually all of the DNA code of the actual genes.
Most of the remaining 3% should be completed within the next few months, said Mark Adams, PhD, of Celera. A small fraction of the genome contains so-called junk DNA, repetitive and noncoding DNA that cannot be sequenced with current technology and which is of considerably less interest to scientists.
"More than 99% of the interesting biological information can be gleaned from the completed sequence," said Gerald Rubin, PhD, who headed the Berkeley group's effort. Much of the raw sequence data is publicly available on the Internet at the National Library of Medicine's GenBank Web site.
Gerald Rubin, PhD, led the Drosophila Genome Project Group at the University of California, Berkeley, effort to decode the fruit fly genome. The group teamed up with Celera Genomics in Rockville, Md, to sequence virtually the entire genome of the fruit fly. (Photo credit: Paul Fetters for Howard Hughes Medical Institute)
The effort revealed that the fruit fly genome comprises more than 13,600 genes, vs the estimated 70,000 to 100,000 genes that comprise the human genetic blueprint. At this point, the function of only about half of Drosophila's genes is known.
Because genetic sequences are often evolutionarily conserved across species, knowing the function of a gene for a model organism such as Drosophila or a mouse can help researchers identify its human equivalent—and vice versa. Finding the counterpart of a known human gene in another organism opens up possibilities of learning more about how such a gene functions in a model organism.
With the new data in hand, the researchers searched for the fruit fly equivalent of 289 human disease gene mutations and found matches for about 60% of them. In one case, for example, the fruit fly equivalent of the human p53 gene, which plays an important role in some human cancers, had eluded attempts of Drosophila researchers to find it. But the fly p53 equivalent "popped right out of the genome," said Adams.
The successful decoding of the fruit fly genome also may quiet skeptics regarding concerns about the usefulness of the whole genome "shotgun" sequencing approach championed by Celera. This technique involves chopping an organism's DNA into a myriad of small pieces; sequencing random, overlapping fragments using automated gene-sequencing equipment; and then using a sophisticated computer algorithm to sort out the information and reassemble the fragments into their proper order.
Areas of the genome that cannot be decoded using automated gene-sequencing equipment are tackled using special sequencing techniques, a process known as finishing.
When J. Craig Venter, PhD, Celera's president, announced in May 1998 that he was forming a company that would use this technique to sequence the human genome, many scientists predicted that the company's researchers would not be able to correctly reassemble the millions of DNA fragments, resulting in a large number of sequence gaps.
However, the approach "worked better than anyone expected," said Rubin.
Stephenson J. Lords of the Fly Decode Drosophila Genome. JAMA. 2000;283(12):1554–1555. doi:10.1001/jama.283.12.1554-JMN0322-2-1
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