期刊
EUKARYOTIC CELL
卷 12, 期 9, 页码 1281-1292出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/EC.00311-12
关键词
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资金
- faculty seed grant from the Constance Miriam and Ethel Corrine Syford Memorial Fund
- Hammond-Maude Fling Fellowship
- Farnesol and Candida albicans Research Fund, University of Nebraska Foundation
- Direct For Biological Sciences
- Div Of Biological Infrastructure [1263302] Funding Source: National Science Foundation
Quorum sensing by farnesol in Candida albicans inhibits filamentation and may be directly related to its ability to cause both mucosal and systemic diseases. The Ras1-cyclic AMP signaling pathway is a target for farnesol inhibition. However, a clear understanding of the downstream effectors of the morphological farnesol response has yet to be unraveled. To address this issue, we screened a library for mutants that fail to respond to farnesol. Six mutants were identified, and the czf1 Delta/czf1 Delta mutant was selected for further characterization. Czf1 is a transcription factor that regulates filamentation in embedded agar and also whiteto-opaque switching. We found that Czf1 is required for filament inhibition by farnesol under at least three distinct environmental conditions: on agar surfaces, in liquid medium, and when embedded in a semisolid agar matrix. Since Efg1 is a transcription factor of the Ras1-cyclic AMP signaling pathway that interacts with and regulates Czf1, an efg1 Delta/efg1 Delta czf1 Delta/czf1 Delta mutant was tested for filament inhibition by farnesol. It exhibited an opaque-cell-like temperature-dependent morphology, and it was killed by low farnesol levels that are sublethal to wild-type cells and both efg1 Delta/efg1 Delta and czf1 Delta/czf1 Delta single mutants. These results highlight a new role for Czf1 as a downstream effector of the morphological response to farnesol, and along with Efg1, Czf1 is involved in the control of farnesol-mediated cell death in C. albicans.
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