SRO9, a Multicopy Suppressor of the Bud Gpowth Defect in the Saccharomyces cerevisiae rho3-Deficient Cells, Shows Strong Genetic Interactions With Tropomyosin Genes, Suggesting Its Role in Organization of the Actin Cytoskeleton
Mitsuhiro Kagami, Akio Toh-e, Yasushi Matsui

Abstract

RHO3 encodes a Rho-type small GTPase in the yeast Saccharomyces cerevisiae and is involved in the proper organization of the actin cytoskeleton required for bud growth. SRO9 (YCL37c) was isolated as a multicopy suppressor of a rho3Δ mutation. An Sro9p domain required for function is similar to a domain in the La protein (an RNA-binding protein). Disruption of SRO9 did not affect vegetative growth, even with the simultaneous disruption of an SRO9 homologue, SRO99. However, sro9Δ was synthetically lethal with a disruption of TPM1, which encodes tropomyosin; sro9Δ tpm1Δ cells did not distribute cortical actin patches properly and lysed. We isolated TPM2, the other gene for tropomyosin, as a multicopy suppressor of a tpm1Δ sro9Δ double mutant. Genetic analysis suggests that TPM2 is functionally related to TPM1 and that tropomyosin is important but not essential for cell growth. Overexpression of SRO9 suppressed the growth defect in tpm1Δ tpm2Δ cells, disappearance of cables of actin filaments in both rho3Δ cells and tpm1Δ cells, and temperature sensitivity of actin mutant cells (act1-1 cells), suggesting that Sro9p has a function that overlaps or is related to tropomyosin function. Unlike tropomyosin, Sro9p does not colocalize with actin cables but is diffusely cytoplasmic. These results suggest that Sro9p is a new cytoplasmic factor involved in the organization of actin filaments.

  • Received March 26, 1997.
  • Accepted July 10, 1997.