Open AccessRad54 and Rdh54 prevent Srs2-mediated disruption of Rad51 presynaptic filaments
Author(s) -
Aviv Meir,
J. Brooks Crickard,
Youngho Kwon,
Patrick Sung,
Eric C. Greene
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2113871119
Subject(s) - rad51 , helicase , microbiology and biotechnology , recombinase , homologous recombination , biology , chemistry , dna , genetics , recombination , gene , rna
Significance Homologous DNA recombination is an essential pathway necessary for the repair of double-stranded DNA breaks. Defects in this pathway are associated with hereditary breast cancer, ovarian cancer, and cancer-prone syndromes. Although essential, too much recombination is also bad and can lead to genetic mutations. Thus, cells have evolved “antirecombinase” enzymes that can actively dismantle recombination intermediates to prevent excessive recombination. However, our current understanding of how antirecombinases are themselves regulated remains very limited. Here, we study the antirecombinase Srs2 and its regulation by the recombination accessory factors Rad54 and Rdh54. Our data suggest that Rad54 and Rdh54 act synergistically to function as key regulators of Srs2, thus serving as “licensing factors” that enable timely progression of DNA repair.