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Switching yeast from meiosis to mitosis: double‐strand break repair, recombination and synaptonemal complex
Author(s) -
Zenvirth Drora,
Loidl Josef,
Klein Shoshana,
Arbel Ayelet,
Shemesh Ronen,
Simchen Giora
Publication year - 1997
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1046/j.1365-2443.1997.1370335.x
Subject(s) - meiosis , rad51 , homologous recombination , synaptonemal complex , biology , homologous chromosome , sister chromatids , genetic recombination , genetics , mitotic crossover , chromosomal crossover , mitosis , dna repair , chromosome segregation , ectopic recombination , chromatid , microbiology and biotechnology , recombination , chromosome , dna , gene
Background: When Saccharomyces cerevisiae cells that have begun meiosis are transferred to mitotic growth conditions (‘return‐to‐growth’, RTG), they can complete recombination at high meiotic frequencies, but undergo mitotic cell division and remain diploid. It was not known how meiotic recombination intermediates are repaired following RTG. Using molecular and cytological methods, we investigated whether the usual meiotic apparatus could repair meiotically induced DSBs during RTG, or whether other mechanisms are invoked when the developmental context changes. Results: Upon RTG, the rapid disappearance of meiotic features—double‐strand breaks in DNA (DSBs), synaptonemal complex (SC), and SC related structures—was striking. In wild‐type diploids, the repair of meiotic DSBs during RTG was quick and efficient, resulting in homologous recombination. Kinetic analysis of double‐strand breakage and recombination indicated that meiotic DSB formation precedes the commitment to meiotic levels of recombination. DSBs were repaired in RTG in dmc1 , but not rad51 mutants, hence repair did not occur by the usual meiotic mechanism which requires the Dmc1 gene product. In haploids, DSBs were also repaired quickly and efficiently upon RTG, showing that DSB repair did not require the presence of a homologous chromosome. In all strains examined, SC and related structures were not required for DSB repair or recombination following RTG. Conclusions: At least two pathways of DSB repair, which differ from the primary meiotic pathway(s), can occur during RTG: One involving interhomologue recombination, and another involving sister‐chromatid exchange. DSB formation precedes commitment to recombination. SC elements appear to prevent sister chromatid exchange in meiosis.