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ShareSep. 24, 2010 — Candida albicans, a fungus that kills more than 10,000 people with weakened immune systems each year, grows more dangerous as it forms and extends long strands of cells called hyphal filaments. In a paper published this month, UT Health Science Center San Antonio microbiologists describe a key factor involved in this damaging growth.
This finding may eventually lead to targets for antifungal strategies, the scientists said.
Patricia Carlisle, a Ph.D. student at the Health Science Center, and David Kadosh, Ph.D., assistant professor of microbiology, found that Ume6, a key transcriptional regulator, targets a specific hyphal filament-development mechanism. "No one knew that Ume6 was involved in directing this process," Dr. Kadosh said. "Perhaps we can learn how to mute its signals."
Transcriptional regulators direct the conversion of DNA (deoxyribonucleic acid) into RNA copies. Copies of RNA (ribonucleic acid) are translated into proteins that carry out activity.
Bug's impact
Candida albicans preys on hospitalized critical care patients, HIV/AIDS patients, cancer patients and others with weakened immune systems. It is the fourth-leading cause of hospital-acquired infections in the United States.
"The forming of hyphal filaments is very important in tissue invasion and other activities," Dr. Kadosh said.
The findings were featured as a Spotlight article in the September issue of Eukaryotic Cell, a journal of the American Society for Microbiology.
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Story Source:
The above story is reprinted from materials provided by University of Texas Health Science Center at San Antonio, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- P. L. Carlisle, D. Kadosh. Candida albicans Ume6, a Filament-Specific Transcriptional Regulator, Directs Hyphal Growth via a Pathway Involving Hgc1 Cyclin-Related Protein. Eukaryotic Cell, 2010; 9 (9): 1320 DOI: 10.1128/EC.00046-10
Note: If no author is given, the source is cited instead.
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