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Related Experiment Videos

Singularity in budding: a role for the evolutionarily conserved small GTPase Cdc42p.

Juliane P Caviston1, Serguei E Tcheperegine, Erfei Bi

  • 1Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

Proceedings of the National Academy of Sciences of the United States of America
|September 10, 2002
PubMed
Summary

Mutant yeast cells with altered Cdc42 protein exhibit uncontrolled budding. This research reveals Cdc42

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Budding yeast Saccharomyces cerevisiae exhibits tightly regulated cell division.
  • The temporal and spatial control of budding is not fully understood.
  • The role of proteins in determining budding frequency remains unclear.

Purpose of the Study:

  • Investigate the molecular mechanisms regulating yeast cell budding.
  • Identify proteins involved in controlling budding frequency.
  • Characterize the function of Cdc42 in polarized growth.

Main Methods:

  • Genetic analysis of cdc42 mutants in Saccharomyces cerevisiae.
  • Biochemical assays to confirm protein hyperactivity.
  • Cellular phenotype analysis of budding patterns.

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Main Results:

  • A specific cdc42 mutation at residue 60 leads to multiple, random buds per cell cycle.
  • This mutation bypasses the need for the guanine-nucleotide-exchange factor Cdc24p.
  • Biochemical data confirmed hyperactivation of Cdc42p due to the mutation.

Conclusions:

  • The activity of Cdc42p is a key determinant of budding frequency.
  • Temporal and spatial regulation of polarized growth converges on Cdc42p.
  • Cdc24p's essential function is likely limited to Cdc42p activation.