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The histone H2B Arg95 residue links the pheromone response pathway to rapamycin-induced G1 arrest in yeast

Abdallah Alhaj Sulaiman1, Reem Ali1, Mustapha Aouida1

  • 1Division of Biological and Biomedical Sciences, College of Health and Life Sciences, Hamad Bin Khalifa University, Education City, Qatar Foundation, P.O. Box: 34110, Doha, Qatar.

Scientific Reports
|June 15, 2022
PubMed

Insights

Rapamycin resistance in yeast involves defective cell cycle arrest. The H2B R95A histone mutant and STE5 deletion show resistance, revealing rapamycin

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Rapamycin is an immunosuppressant that inhibits the TORC1 kinase signaling pathway.
  • Rapamycin causes cell cycle arrest in G1, but the mechanisms are not fully understood.
  • Histone modifications can influence cellular responses to rapamycin.

Purpose of the Study:

  • To investigate the role of histone mutations in rapamycin sensitivity.
  • To elucidate the mechanisms of rapamycin-induced cell cycle arrest.
  • To identify novel pathways involved in rapamycin signaling.

Main Methods:

  • Screening of a histone mutant collection for rapamycin resistance.
  • Analysis of gene expression in wild-type and mutant yeast strains.
  • Assessing cell cycle progression and arrest.
  • Investigating the pheromone pathway and MAPK activation.

Main Results:

  • The H2B R95A histone mutant exhibits resistance to rapamycin due to defective G1 cell cycle arrest.
  • This resistance is linked to reduced expression of genes in the pheromone pathway, including STE5.
  • Cells lacking Ste5 are also resistant to rapamycin, and rapamycin treatment induces Cln2 expression.
  • Rapamycin-induced G1 arrest does not involve detectable phosphorylation of MAPKs Kss1 and Fus3.

Conclusions:

  • Rapamycin signaling may utilize the pheromone pathway to induce G1 cell cycle arrest.
  • Histone H2B, specifically residue R95, plays a role in mediating this response.
  • The findings offer new insights into the complex mechanisms of rapamycin action.

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