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Three Different Pathways Prevent Chromosome Segregation in the Presence of DNA Damage or Replication Stress in

Gloria Palou1, Roger Palou1, Fanli Zeng1

  • 1Department of Biochemistry and Molecular Biology, Biophysics Unit, School of Medicine, Universitat Autonoma de Barcelona, Bellaterra, Catalonia, Spain.

Plos Genetics
|September 3, 2015
PubMed

Insights

The S phase checkpoint prevents mitosis during DNA damage. In budding yeast, Swe1 (a Wee1 ortholog) inhibits mitosis, but this is redundant due to Rad53, preventing genomic instability.

Area of Science:

  • Cell cycle regulation
  • DNA damage response
  • Genomic stability

Background:

  • The S phase checkpoint is crucial for preventing genomic instability by halting cell cycle progression during DNA damage or replication stress.
  • Inhibition of mitotic cyclin-dependent kinase (M-CDK) by Wee1 kinases is a key mechanism for blocking mitosis in response to genotoxic stress in some organisms.
  • This Wee1-dependent mechanism is considered dispensable in the model eukaryote Saccharomyces cerevisiae.

Purpose of the Study:

  • To investigate the role of the Wee1 ortholog, Swe1, in the S phase checkpoint response to genotoxic stress in Saccharomyces cerevisiae.
  • To elucidate the mechanisms underlying Swe1's function and its relationship with other checkpoint proteins, such as Rad53 and Mec1.
  • To understand how disruption of checkpoint controls leads to aberrant chromosome segregation.

Main Methods:

  • Utilized the model eukaryotic organism Saccharomyces cerevisiae.
  • Investigated the function of Swe1, a Wee1 ortholog, in response to genotoxic insults.
  • Analyzed the interplay between Swe1, Rad53, Mec1, and Pds1/securin in controlling M-CDK activity and chromosome segregation.

Main Results:

  • Demonstrated that Swe1 inhibits M-CDK activity and chromosome segregation in response to genotoxic stress in budding yeast.
  • Revealed that Swe1's apparent dispensability in budding yeast is due to redundant M-CDK control by the checkpoint kinase Rad53.
  • Showed that Swe1 acts as an effector of the central checkpoint kinase Mec1.
  • Observed aberrant chromosome segregation when checkpoint control on M-CDK and Pds1/securin stabilization was abrogated.

Conclusions:

  • Swe1 plays a significant role in blocking mitosis and maintaining genomic stability during genotoxic stress in budding yeast.
  • Redundancy between Swe1 and Rad53 provides a robust checkpoint mechanism in Saccharomyces cerevisiae.
  • Mec1-dependent regulation of Swe1 is critical for the DNA damage response pathway.

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