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1 Department of Microbiology, Columbia University, 701 West 168th Street, NY 10032, USA
2 Biological Sciences Program, Department of Biological Sciences, Columbia University, NY 10027, USA
3 Integrated Program in Cellular, Molecular and Biophysical Studies, Columbia University, NY 10032, USA
Correspondence
Aaron P. Mitchell
apm4{at}columbia.edu
The chlamydospore is a distinctive morphological feature of the fungal pathogen Candida albicans that can be induced to form in oxygen-limited environments and has been reported in clinical specimens. Chlamydospores are not produced by the model yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe, so there is limited understanding of the pathways that govern their development. Here, the results of a forward genetic approach that begins to define the genetic control of chlamydospore formation are described. Six genes – ISW2, MDS3, RIM13, RIM101, SCH9 and SUV3 – are required for efficient chlamydospore formation, based on the phenotypes of homozygous insertion mutants and reconstituted strains. Mutations in ISW2, SCH9 and SUV3 completely abolish chlamydospore formation. Mutations in RIM13, RIM101 and MDS3 delay normal chlamydospore formation. The involvement of alkaline pH-response regulators Rim13p and Mds3p in chlamydospore formation is unexpected in view of the fact that chlamydospores in the inducing conditions used here are repressed in alkaline media.
Present address: Department of Microbiology, University of Minnesota, MN 55455, USA.
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