Abstract |
Candida albicans, a fungus that normally inhabits the digestive tract and other mucosal surfaces, can become a pathogen in immunocompromised individuals, causing severe or even fatal infection. Mechanisms by which C. albicans can evade commonly used antifungal agents are not fully understood. We are studying a model system involving growth of C. albicans on toxic sugar sorbose, which represses synthesis of cell wall glucan and, as a result, kills fungi in a manner similar to drugs from the echinocandins class. Adaptation to sorbose occurs predominantly due to reversible loss of one homolog of chromosome 5 (Ch5), which results in upregulation of the metabolic gene SOU1 ( SOrbose Utilization) on Ch4. Here, we show that growth on sorbose due to Ch5 monosomy can involve a facultative trisomy of a hybrid Ch4/7 that serves to increase copy number of the SOU1 gene. This shows that control of expression of SOU1 can involve multiple mechanisms; in this case, negative regulation and increase in gene copy number operating simultaneously in cell.
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Authors | Anatoliy Kravets, Feng Yang, Gabor Bethlendy, Yongbing Cao, Fred Sherman, Elena Rustchenko |
Journal | FEMS yeast research
(FEMS Yeast Res)
Vol. 14
Issue 5
Pg. 708-13
(Aug 2014)
ISSN: 1567-1364 [Electronic] England |
PMID | 24702787
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Copyright | © 2014 Federation of European Microbiological Societies. Published by John Wiley & Sons Ltd. All rights reserved. |
Chemical References |
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Topics |
- Adaptation, Biological
- Candida albicans
(genetics, growth & development, metabolism)
- Chromosomes, Fungal
- Gene Expression Regulation, Fungal
- Monosomy
- Sorbose
(metabolism, toxicity)
- Trisomy
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