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The MBR1 gene from Saccharomyces cerevisiae is activated by and required for growth under sub-optimal conditions

P Reisdorf1, E Boy-Marcotte, M Bolotin-Fukuhara

  • 1Institut de Génétique et Microbiologie, URA CNRS D1354, Université Paris-Sud, Orsay, France.

Molecular & General Genetics : MGG
|July 1, 1997
PubMed

Insights

The MBR1 gene is crucial for yeast growth under stress. Deleting MBR1 enhances stress protection, while its overexpression is detrimental, suggesting a role in cellular stress response.

Area of Science:

  • Molecular biology
  • Yeast genetics

Background:

  • The MBR1 gene was identified as a suppressor of growth defects in Saccharomyces cerevisiae lacking the Hap2/3/4/5 transactivator complex.
  • Understanding MBR1's function is key to comprehending yeast's adaptation to various environmental conditions.

Purpose of the Study:

  • To investigate the role of the MBR1 gene in Saccharomyces cerevisiae growth and stress response.
  • To elucidate the regulatory mechanisms controlling MBR1 expression and its interaction with other cellular pathways.

Main Methods:

  • Genetic analysis of MBR1 deletion and overexpression mutants.
  • Phenotypic analysis under various sub-optimal growth conditions (glycerol medium, late growth phase, low temperature, high pH, 1,10-phenanthroline).
  • Investigating the relationship between MBR1, protein kinase A (PKA), SOK1, SCH9, and SAC1.

Main Results:

  • Mbr1p is a limiting factor for yeast growth on glycerol under stress conditions.
  • MBR1 deletion confers stress protection, whereas MBR1 overexpression sensitizes cells to stress.
  • MBR1 expression is induced during late growth and negatively regulated by PKA.
  • MBR1 deletion exhibits synthetic lethality with SAC1 deletion, suggesting a role in intracellular trafficking.

Conclusions:

  • Mbr1p plays a significant role in yeast stress response and adaptation.
  • The MBR1 gene is regulated by PKA and involved in pathways beyond the Hap2/3/4/5 complex.
  • Mbr1p may be implicated in intracellular trafficking pathways, as suggested by its interaction with SAC1.

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