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Related Experiment Videos

Cell wall integrity modulates RHO1 activity via the exchange factor ROM2

M Bickle1, P A Delley, A Schmidt

  • 1Department of Biochemistry, Biozentrum, University of Basel, Klingelbergstrasse 70, CH-4056 Basel, Switzerland.

The EMBO Journal
|May 26, 1998
PubMed
Summary

Cell wall defects in Saccharomyces cerevisiae suppress TOR2 mutations by activating RHO1, promoting actin cytoskeleton polarization and cell wall synthesis independently of TOR2.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Genetics

Background:

  • The TOR2 protein kinase regulates the actin cytoskeleton in Saccharomyces cerevisiae via the RHO1 GTPase switch.
  • Understanding the pathways that control cell wall integrity and their relationship with TOR signaling is crucial for yeast cell biology.

Purpose of the Study:

  • To investigate the relationship between cell wall integrity and TOR2-mediated actin cytoskeleton regulation.
  • To identify novel genes and pathways involved in suppressing TOR2 loss-of-function mutations.

Main Methods:

  • Genetic screening for suppressors of tor2 mutations.
  • Isolation and characterization of suppressor genes (ROT1, ROT2, BIG1).
  • Biochemical assays to measure RHO1 GTPase activity.
  • Phenotypic analysis of yeast mutants with cell wall defects.

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Main Results:

  • Identified rot1 and rot2 mutations that suppress tor2 loss-of-function and are synthetically lethal.
  • Isolated ROT1, ROT2 (encoding glucosidase II), and BIG1 as suppressors.
  • Demonstrated that cell wall defects, induced by mutations or SDS treatment, suppress tor2 mutations.
  • Showed that cell wall defects activate RHO1 GTPase activity independently of TOR2, leading to actin polarization.

Conclusions:

  • Cell wall defects suppress tor2 mutations by activating RHO1 through the ROM2 exchange factor, independent of TOR2.
  • This activation leads to TOR2-independent actin cytoskeleton polarization and cell wall synthesis.
  • Suggests a mechanism where cell wall integrity signals activate RHO1 to ensure localized cell wall synthesis, analogous to mammalian integrin signaling.