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Microbiology 155 (2009), 3847-3859; DOI  10.1099/mic.0.033233-0
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Microbiology 155 (2009), 3847-3859; DOI  10.1099/mic.0.033233-0
© 2009 Society for General Microbiology

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

Cheryl A. Gale1,2, Michelle D. Leonard2,{dagger}, Kenneth R. Finley2,{ddagger}, Leah Christensen2,§, Mark McClellan2, Darren Abbey2, Cornelia Kurischko2,3, Eric Bensen2,||, Iris Tzafrir2, Sarah Kauffman4, Jeff Becker4 and Judith Berman2,5

1 Department of Pediatrics, University of Minnesota, Minneapolis MN 55455, USA
2 Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, MN 55455, USA
3 Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
4 Department of Microbiology, University of Tennessee, Knoxville, TN 37996, USA
5 Department of Microbiology, University of Minnesota, Minneapolis, MN 55455, USA

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.

Correspondence
Judith Berman
jberman{at}umn.edu


Abbreviations: DAPI, 4',6-diamidino-2-phenylindole; DIC, differential interference contrast; GFP, green fluorescent protein; HA, haemagglutinin; YFP, yellow fluorescent protein

{dagger}Present address: Hennepin County Sheriff's Office-Crime Laboratory, 531 Park Ave S., Minneapolis, MN 55415, USA.

{ddagger}Present Address: Cargill, Bio TDC-Bioindustrials, 15285 Minnetonka Blvd, Minnetonka, MN 55345, USA.

§Present address: Laboratory of Persistent Viral Diseases, NIAID, NIH, Rocky Mountain Laboratories, 903 South 4th St, Hamilton, MT 59840, USA.

||Present address: MD Biosciences, Inc., 1000 Westgate Dr, Suite 162, St Paul, MN 55114, USA.

Present address: Syngenta Seeds Inc., 7500 Olson Memorial Hwy, Golden Valley, MN 55427, USA.

Two supplementary movies and two supplementary figures are available with the online version of this paper.




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S. D. Harris
Special issue: Physiology and Systems Biology of the Fungal Cell
Microbiology, December 1, 2009; 155(12): 3797 - 3798.
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