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MAPK mediated cell cycle regulation is associated with Cdc25 turnover in S. pombe after exposure to genotoxic stress

Geetanjali Sundaram1, Santanu Palchaudhuri, Swati Dixit

  • 1B. C. Guha Centre for Genetic Engineering and Biotechnology, Department of Biochemistry, University of Calcutta, Kolkata, India.

Cell Cycle (Georgetown, Tex.)
|February 1, 2008
PubMed

Insights

Cigarette smoke extract activates stress response pathways in fission yeast. The study reveals a novel interaction between MAPK Sty1 and Cdc25, preventing cell division and regulating cell cycle checkpoints.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Carcinogens like cigarette smoke induce genotoxic stress.
  • This stress activates the MAPK pathway and S phase checkpoint in Schizosaccharomyces pombe.
  • The crosstalk between these pathways is not well understood.

Purpose of the Study:

  • To investigate the molecular mechanisms coordinating the MAPK and S phase checkpoint pathways.
  • To identify common effector molecules and interactions between these pathways.
  • To understand how cigarette smoke extract (CSE) induced stress is managed in fission yeast.

Main Methods:

  • Utilized Schizosaccharomyces pombe as a model organism.
  • Investigated the interaction between MAPK Sty1 and Cdc25.
  • Assessed the role of Rad3 activity in Cdc25 turnover.
  • Analyzed cell cycle progression and checkpoint activation.

Main Results:

  • Identified Cdc25 as a common effector molecule for both pathways.
  • Demonstrated that MAPK Sty1 directly interacts with Cdc25, inhibiting mitotic entry upon CSE exposure.
  • Showed that Cdc25 turnover after CSE treatment depends on Rad3 activity and Sty1-Cdc25 interaction.
  • Confirmed Sty1 activity is not essential for S phase checkpoint activation.

Conclusions:

  • CSE-induced stress triggers a coordinated response involving both S phase and mitotic checkpoints.
  • The interaction between Sty1 and Cdc25 is crucial for managing CSE-induced stress and regulating cell cycle progression.
  • This study provides the first evidence of Sty1-Cdc25 interaction in S. pombe, elucidating a key mechanism in cellular stress response.

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