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A more recent version of this article appeared on June 1, 2005 Originally published as MBC in Press, 10.1091/mbc.E05-01-0079 on April 15, 2005
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Submitted on January 31, 2005
Revised on March 23, 2005
Accepted on March 24, 2005
Department of Molecular Microbiology, B. Rappaport Faculty of Medicine, Technion-I.I.T. and the Rappaport Institute for Research in the Medical Sciences, Haifa 31096, Israel
Monitoring Editor: Orna Cohen-Fix
The ability of C. albicans, a major fungal pathogen, to switch between a yeast form, and a hyphal (mold) form is recognized as being important for the ability of the organism to invade the host and cause disease. We found that a C. albicans mutant deleted for CaCDC4, a homolog of the S. cerevisiae F-box protein component of the SCFCDC4 ubiquitin ligase, is viable and displays constitutive filamentous, mostly hyphal, growth. The phenotype of the Cacdc4-/- mutant suggests that ubiquitin-mediated protein degradation is involved in the regulation of the dimorphic switch of C. albicans, and that one or more regulators of the yeast-to-mold switch are among the substrates of SCFCaCDC4. Epistasis analysis indicates that the Cacdc4-/- phenotype is largely independent of the filamentation-inducing transcription factors Efg1 and Cph1. We identify C. albicans Far1 and Sol1, homologues of the S. cerevisiae SCFCDC4 substrates Far1 and Sic1, and show that Sol1 is a substrate of C. albicans Cdc4. Neither protein is essential for the hyphal phenotype of the Cacdc4-/- mutant. However, ectopic expression and deletion of SOL1 indicate a role for this gene in C. albicans morphogenesis.
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