The Rho1 effector Pkc1, but not Bni1, mediates signalling from Tor2 to the actin cytoskeleton

Curr Biol. 1998 Nov 5;8(22):1211-4. doi: 10.1016/s0960-9822(07)00511-8.

Abstract

In Saccharomyces cerevisiae, the phosphatidylinositol kinase homologue Tor2 controls the cell-cycle-dependent organisation of the actin cytoskeleton by activating the small GTPase Rho1 via the exchange factor Rom2 [1,2]. Four Rho1 effectors are known, protein kinase C 1 (Pkc1), the formin-family protein Bni1, the glucan synthase Fks and the signalling protein Skn7 [2,3]. Rho1 has been suggested to signal to the actin cytoskeleton via Bni1 and Pkc1; rho1 mutants have never been shown to have defects in actin organisation, however [2,4]. We have further investigated the role of Rho1 in controlling actin organisation and have analysed which of the Rho1 effectors mediates Tor2 signalling to the actin cytoskeleton. We show that some, but not all, rho1 temperature-sensitive (rho1ts) mutants arrest growth with a disorganised actin cytoskeleton. Both the growth defect and the actin organisation defect of the rho1-2ts mutant were suppressed by upregulation of Pkc1 but not by upregulation of Bni1, Fks or Skn7. Overexpression of Pkc1, but not overexpression of Bni1, Fks or Skn7, also rescued a tor2ts mutant, and deletion of BNI1 or SKN7 did not prevent the suppression of the tor2ts mutation by overexpressed Rom2. Furthermore, overexpression of the Pkc1-controlled mitogen-activated protein (MAP) kinase Mpk1 suppressed the actin defect of tor2ts and rho1-2ts mutants. Thus, Tor2 signals to the actin cytoskeleton via Rho1, Pkc1 and the cell integrity MAP kinase cascade.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / physiology*
  • Cell Cycle Proteins
  • Cell Division
  • Cytoskeleton / physiology*
  • DNA-Binding Proteins / genetics
  • Echinocandins
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism*
  • GTP Phosphohydrolases / genetics
  • GTP Phosphohydrolases / metabolism*
  • GTP-Binding Proteins / genetics
  • GTP-Binding Proteins / metabolism*
  • Glucosyltransferases*
  • MAP Kinase Kinase 1
  • MAP Kinase Kinase 2
  • Membrane Proteins / genetics
  • Microfilament Proteins*
  • Mitogen-Activated Protein Kinase Kinases*
  • Mutagenesis
  • Phosphatidylinositol 3-Kinases
  • Phosphotransferases (Alcohol Group Acceptor) / genetics
  • Phosphotransferases (Alcohol Group Acceptor) / metabolism*
  • Protein Kinase C*
  • Protein Kinases / genetics
  • Protein-Serine-Threonine Kinases / genetics
  • Protein-Tyrosine Kinases / genetics
  • Saccharomyces cerevisiae / genetics
  • Saccharomyces cerevisiae / metabolism
  • Saccharomyces cerevisiae / physiology
  • Saccharomyces cerevisiae Proteins*
  • Signal Transduction*
  • Transcription Factors / genetics
  • rho GTP-Binding Proteins*

Substances

  • Actins
  • Bni1 protein, S cerevisiae
  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Echinocandins
  • Fungal Proteins
  • Membrane Proteins
  • Microfilament Proteins
  • SKN7 protein, S cerevisiae
  • Saccharomyces cerevisiae Proteins
  • Transcription Factors
  • Glucosyltransferases
  • FKS1 protein, S cerevisiae
  • Protein Kinases
  • Phosphotransferases (Alcohol Group Acceptor)
  • Pkc1 protein, Trichoderma reesei
  • TOR2 protein, S cerevisiae
  • Protein-Tyrosine Kinases
  • BCK1 protein, S cerevisiae
  • Protein-Serine-Threonine Kinases
  • Protein Kinase C
  • MAP Kinase Kinase 1
  • MAP Kinase Kinase 2
  • Mitogen-Activated Protein Kinase Kinases
  • GTP Phosphohydrolases
  • GTP-Binding Proteins
  • RHO1 protein, S cerevisiae
  • rho GTP-Binding Proteins