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MMS1 protects against replication-dependent DNA damage in Saccharomyces cerevisiae

T Hryciw1, M Tang, T Fontanie

  • 1Department of Microbiology and Immunology, University of Saskatchewan, Saskatoon, SK, Canada, S7K 0M7.

Molecular Genetics and Genomics : MGG
|January 26, 2002
PubMed

Insights

The MMS1 gene protects yeast cells from DNA damage caused by methyl methanesulfonate (MMS). This MMS1-dependent pathway, involving Rad52, is crucial for preventing replication-dependent DNA damage and genomic instability.

Area of Science:

  • Molecular Biology
  • Genetics
  • DNA Repair

Background:

  • Methyl methanesulfonate (MMS) is a monofunctional DNA-alkylating agent.
  • Yeast mutants sensitive to MMS but not UV or X-radiation were isolated.
  • The MMS1 gene was identified and characterized.

Purpose of the Study:

  • To investigate the function of the MMS1 gene in DNA damage response.
  • To elucidate the role of Mms1 in protecting yeast cells from genotoxic agents.
  • To understand the relationship between Mms1 and the Rad52 DNA repair pathway.

Main Methods:

  • Isolation and characterization of yeast mutants.
  • Gene cloning and characterization of MMS1.
  • Sensitivity assays using MMS, UV, camptothecin, and gamma-rays.
  • Epistasis analysis with rad52 Delta mutants.

Main Results:

  • mms1 Delta mutants exhibit extreme sensitivity to MMS and mild sensitivity to UV radiation.
  • mms1 Delta mutants show increased spontaneous DNA damage and genomic instability.
  • Sensitivity to replication-dependent double-strand breaks (camptothecin, cdc2-2 strain) was observed in mms1 Delta cells.
  • Mms1 acts in concert with Rad52, as indicated by epistasis analysis.
  • mms1 Delta cells are not sensitive to gamma-rays, suggesting a replication-dependent mechanism.

Conclusions:

  • Mms1 plays a critical role in the DNA damage response pathway in yeast.
  • An Mms1-dependent, Rad52-mediated pathway protects against replication-dependent DNA damage.
  • This pathway is distinct from pathways responding to replication-independent double-strand breaks like those induced by gamma-rays.

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