Genetic interactions with RVS161 and RVS167.
Helena Friesen, Christine Humphries, Oliver Schub, Brenda Andrews
Dept. of Medical Genetics, University of Toronto, 1 King's College Cir, Toronto, M5S 1A8, Canada
Rvs161 and Rvs167 are required for proper polarization of the actin cytoskeleton, endocytosis, sporulation, and cell survival following starvation. The phenotype of the rvs161 mutant is identical to that of the rvs167 mutant except that RVS161 has a role in cell fusion during mating. Both Rvs161 and Rvs167 have N-terminal BAR domains through which the two proteins interact. Rvs167 has a C-terminal SH3 domain; however the SH3 is not required to complement any rvs167 defect. Our genetic analysis reveals that RVS161 and RVS167 have an identical set of 50 synthetic lethal interactions and suggests novel roles for the Rvs proteins in cell polarity, cell wall synthesis and integrity, and vesicle trafficking. We find that the transcriptional regulation of PKC pathway/Swi4 and of Sin3/Rpd3 targets is essential in the absence of RVS genes. In addition, we have identified several genetic combinations that cause mating defects in an rvs161 background. Only a subset of these mutants cause mating defects in combination with rvs167. We have tested whether the SH3 domain of Rvs167 is required to complement the rvs167 double mutants. We present the first genetic evidence for a role for the Rvs167 SH3 domain: the Rvs167 SH3-mediated interaction with Abp1 is important in the absence of the actin cytoskeleton protein, Sla1. We conclude that the biological roles of Rvs161 and Rvs167 are identical during vegetative growth and have subtle differences during mating.
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