Homologous recombination is essential for RAD51 up-regulation in Saccharomyces cerevisiae following DNA crosslinking damage | Zendy

Yuval Cohen | Zendy

Open Access

Homologous recombination is essential for RAD51 up-regulation in Saccharomyces cerevisiae following DNA crosslinking damage

Author(s) -

Yuval Cohen

Publication year - 2002

Publication title -

nucleic acids research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 9.008

H-Index - 537

eISSN - 1362-4954

pISSN - 0305-1048

DOI - 10.1093/nar/30.5.1224

Subject(s) - rad51 , biology , homologous recombination , dna repair , dna damage , homology directed repair , saccharomyces cerevisiae , mutant , non homologous end joining , dna , replication protein a , nucleotide excision repair , flp frt recombination , dna repair protein xrcc4 , microbiology and biotechnology , genetics , gene , genetic recombination , recombination , dna binding protein , transcription factor

We have determined the kinetics of up-regulation of the homologous recombination gene RAD51, one of the genes induced following DNA damage in isogenic haploid DNA repair-deficient mutants of Saccharomyces cerevisiae, using treatment with the DNA crosslinking agent 8-methoxypsoralen. We show that RAD51 is up-regulated concomitantly, although independently, with a shift from the G1 cell cycle phase to G2/M arrest. This up-regulation is absent in homologous recombination repair-deficient mutants and increased in mutants deficient in nucleotide excision repair and pol(zeta)-dependent translesion synthesis. We demonstrate that the Rad53-dependent DNA damage signal transduction cascade is active in RAD51 non-inducing mutants. However, when independently eliminated, it too abolishes RAD51 up-regulation. We present a model in which RAD51 up-regulation requires two signals: one depending on the Rad53-dependent DNA damage signal transduction cascade and the other on homologous recombination repair.

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