Residual double strand break repair during meiosis in budding yeast is promoted by PIF1, RAD54 and RDH54/TID1

Raunak Dutta1, Lihong Wan1, David Murtha1

  • 1Department of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, NY 11794-5215,United States.

Genetics
|May 7, 2026
PubMed

Insights

Researchers studied double-strand break repair in yeast meiosis. They found RDH54/TID1 partially compensates for RAD54, while PIF1 acts independently in this crucial DNA repair process.

Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Meiosis involves programmed double-strand breaks (DSBs) for homologous recombination.
  • DSB repair in Saccharomyces cerevisiae occurs in two phases during prophase I.
  • Phase 1 is Dmc1-mediated, facilitating synapsis, followed by Phase 2 Rad51-mediated repair.

Purpose of the Study:

  • To investigate the roles of RAD54, RDH54/TID1, and PIF1 in Phase 2 meiotic recombination.
  • To overcome challenges in studying the low frequency of DSBs during pachynema.

Main Methods:

  • Development of a novel method for analyzing Phase 2 recombination.
  • Utilizing budding yeast (Saccharomyces cerevisiae) as a model organism.

Main Results:

  • RDH54/TID1 was found to partially compensate for RAD54 function in Phase 2 repair.
  • PIF1 demonstrated independent function, not relying on RAD54 or RDH54/TID1 for its role.
  • The study provides new insights into the complex genetic regulation of meiotic recombination.

Conclusions:

  • RAD54, RDH54/TID1, and PIF1 play distinct roles in the repair of residual DSBs during meiotic prophase I.
  • Understanding these repair pathways is critical for ensuring genomic stability during meiosis.

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