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TOR signalling regulates mitotic commitment through stress-activated MAPK and Polo kinase in response to nutrient

Janni Petersen1

  • 1University of Manchester, Michael Smith Building, Faculty of Life Sciences, Oxford Road, Manchester M13 9PT, UK. Janni.Petersen@manchester.ac.uk

Biochemical Society Transactions
|January 16, 2009
PubMed

Insights

Nutrient availability controls cell size by coupling growth and division. Stress-activated pathways, like target of rapamycin (TOR) and mitogen-activated protein kinase (MAPK), interact to regulate cell division timing and commitment, particularly in fission yeast.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Yeast Genetics

Background:

  • Cell growth and division are coordinated to maintain cell size, influenced by nutrient availability.
  • The target of rapamycin (TOR) pathway links nutrient sensing to cell growth and division.
  • Environmental changes often activate stress-activated mitogen-activated protein kinase (MAPK) pathways, which also regulate cell division.

Purpose of the Study:

  • To discuss the interplay between TOR and stress MAPK signaling pathways.
  • To elucidate the control of mitotic commitment by these pathways.
  • To focus on the model organism, fission yeast (Schizosaccharomyces pombe).

Main Methods:

  • Literature review and discussion.
  • Focus on signaling pathway analysis.
  • Comparative study using fission yeast as a model.

Main Results:

  • Nutrient stress inhibits TOR signaling, advancing cell division timing.
  • This leads to cell division at a reduced cell size.
  • Stress-activated MAPK pathways play a role in controlling mitotic onset.

Conclusions:

  • TOR and stress MAPK pathways interact to control mitotic commitment.
  • This interplay is crucial for regulating cell size and division in response to environmental cues.
  • Fission yeast serves as a valuable model for studying these fundamental cellular processes.

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