Progress, and Applications
of the Human Genome Project
Sponsored by the U.S. Department of Energy Human Genome Program
Human Genome News Archive Edition
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In the News
Genetics in Medicine
Chlamydia Genome Offers Surprises
Stimulates New Research into Treatment of Major STD, Prevention of Blindness
Analysis of the 1-Mb genome of Chlamydia trachomatis has revealed some unexpected biology for the tiny organism. C. trachomatis is responsible for causing the most common bacterial sexually transmitted disease (STD) in the United States as well as trachoma, a major cause of blindness in Asia and Africa. A collaboration among scientists at the University of California at Berkeley and Stanford University, the study was reported in the genome issue of Science (October 23, 1998).
Of 18 fully sequenced bacterial genomes, Chlamydia is the only obligate intracellular parasite, growing exclusively within eukaryotic cells and requiring host enzymes and cellular machinery for several necessary functions. Researchers were surprised to learn that it harbors genes that could allow it to generate its own energy-storage molecule, ATP (adenosine triphosphate).
Another new finding explained why Chlamydia is vulnerable to penicillin. Although Chlamydia was thought to lack peptidoglycan, a vital bacterial cell-wall component and the antibiotic's major target, scientists have identified the genes for synthesizing this molecule. Other genes found for new surface proteins may be important for future vaccine development, possibly by using the gene sequence itself instead of the protein to stimulate an immune response. Data are available on the Chlamydia Genome Project Web site
The project is focusing now on sequencing the genome of the organism C. pneumoniae, which causes a mild pneumonia and also may contribute to the development of atherosclerotic lesions. This project is funded by the genome data company Incyte Pharmaceuticals (Palo Alto, California), which also is sequencing human genes (p. 7). [Denise Casey, HGMIS]
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Last modified: Wednesday, October 29, 2003
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