1. SLA2 mutations cause SWE1-mediated cell cycle phenotypes in Candida albicans and Saccharomyces cerevisiae
- Author
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Jeff Becker, Cheryl A. Gale, Mark McClellan, Michelle D. Leonard, Cornelia Kurischko, Judith Berman, Kenneth R. Finley, Eric S. Bensen, Darren Abbey, Leah Christensen, Sarah Kauffman, and Iris Tzafrir
- Subjects
Male ,Saccharomyces cerevisiae Proteins ,Endocytic patch ,Genes, Fungal ,Endocytic cycle ,Saccharomyces cerevisiae ,Morphogenesis ,Cell Cycle Proteins ,macromolecular substances ,Microbiology ,Fungal Proteins ,Mice ,Candida albicans ,Animals ,DNA, Fungal ,Cytoskeleton ,Cell Cycle Protein ,DNA Primers ,Mice, Inbred ICR ,Base Sequence ,Virulence ,biology ,Cell Cycle ,Candidiasis ,Protein-Tyrosine Kinases ,Cell cycle ,biology.organism_classification ,Molecular biology ,Actins ,Endocytosis ,Cell biology ,Cytoskeletal Proteins ,Disease Models, Animal ,Mutation ,Gene Deletion ,Physiology and Systems Biology of the Fungal Cell ,Plasmids - Abstract
The early endocytic patch protein Sla2 is important for morphogenesis and growth rates inSaccharomyces cerevisiaeandCandida albicans,but the mechanism that connects these processes is not clear. Here we report that growth defects in cells lacking CaSLA2or ScSLA2are 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. Onlysla2strains 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 ofC. albicansinfections.
- Published
- 2009
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