Rad54 and Rdh54 prevent Srs2-mediated disruption of Rad51 presynaptic filaments

Abstract

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.