SLA2 mutations cause SWE1-mediated cell cycle phenotypes in Candida albicans and Saccharomyces cerevisiae

Cheryl A Gale, Michelle D. Leonard, Kenneth R. Finley, Leah Christensen, Mark McClellan, Darren Abbey, Cornelia Kurischko, Eric Bensen, Iris Tzafrir, Sarah Kauffman, Jeff Becker, Judith Berman

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

The early endocytic patch protein Sla2 is important for morphogenesis and growth rates in Saccharomyces cerevisiae and Candida albicans, but the mechanism that connects these processes is not clear. Here we report that growth defects in cells lacking CaSLA2 or ScSLA2 are associated with a cell cycle delay that is influenced by Swe1, a morphogenesis checkpoint kinase. To establish how Swe1 monitors Sla2 function, we compared actin organization and cell cycle dynamics in strains lacking other components of early endocytic patches (Sla1 and Abp1) with those in strains lacking Sla2. Only sla2 strains had defects in actin cables, a known trigger of the morphogenesis checkpoint, yet all three strains exhibited Swe1-dependent phenotypes. Thus, Swe1 appears to monitor actin patch in addition to actin cable function. Furthermore, Swe1 contributed to virulence in a mouse model of disseminated candidiasis, implying a role for the morphogenesis checkpoint during the pathogenesis of C. albicans infections.

Original languageEnglish (US)
Pages (from-to)3847-3859
Number of pages13
JournalMicrobiology
Volume155
Issue number12
DOIs
StatePublished - 2009

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