Journal
SCIENCE
Volume 337, Issue 6100, Pages 1353-1356Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1224339
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Funding
- Canadian Institutes of Heath Research [MOP-97939]
- Natural Sciences and Engineering Research Council (NSERC) of Canada [RGPIN 204899-05]
- Howard Hughes Medical Institute Research Scholar
- Burroughs Wellcome Fund
- Canada Research Chair in Microbial Genomics and Infectious Disease
- NSERC [355965-2009]
- NIH [GM40266, GM035010]
- National Human Genome Research Institute
- European Molecular Biology Organization
- Austrian Science Fund (FWF) [I 746] Funding Source: researchfish
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [0919787] Funding Source: National Science Foundation
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The dimorphic switch from a single-cell budding yeast to a filamentous form enables Saccharomyces cerevisiae to forage for nutrients and the opportunistic pathogen Candida albicans to invade human tissues and evade the immune system. We constructed a genome-wide set of targeted deletion alleles and introduced them into a filamentous S. cerevisiae strain, Sigma 1278b. We identified genes involved in morphologically distinct forms of filamentation: haploid invasive growth, biofilm formation, and diploid pseudohyphal growth. Unique genes appear to underlie each program, but we also found core genes with general roles in filamentous growth, including MFG1 (YDL233w), whose product binds two morphogenetic transcription factors, Flo8 and Mss11, and functions as a critical transcriptional regulator of filamentous growth in both S. cerevisiae and C. albicans.
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