Abstract
The efficient repair of chromosome breaks by homologous recombination depends on the ability of the ends of a double‐strand break (DSB) to locate homologous sequences to serve as templates to repair the lesion. These repair mechanisms are conserved across eukaryotic evolution. Repair depends on 5’ to 3’ resection of the broken ends, allowing the assembly of a Rad51 filament. In yeast, fruit flies, and mammals, broken chromosome ends display increased mobility, allowing the ends to explore a larger volume. The Arp2/3 actin nucleator complex plays a key role in increased local chromatin mobility near a DSB. In budding yeast, Arp2/3, LAS17WASP, and myosins are required both to initiate and to maintain long‐range end resection, affecting both DNA repair and the maintenance of the DNA damage checkpoint. At least in budding yeast, the connection between controlling long‐range resection and increased mobility is direct, as inhibiting resection prevents damage‐induced chromatin mobility. Moreover, although the search for homology by Rad51‐coated broken DNA ends would seem to be improved by greater exploration of the nuclear volume, increased local mobility through Arp2/3 per se does not affect the efficiency of ectopic recombination in yeast. Here, we review the recently defined roles of nuclear actin in DNA damage repair, with a focus on new observations in budding yeast. Arp2/3 has an evolutionarily conserved role in promoting 5’ to 3’ resection of DSBs, RAD51 filament formation, maintenance of the DNA damage checkpoint, increased mobility of DSBs, and relocation of damage in heterochromatin regions to the nuclear periphery. This activity is mediated by myosin proteins and Las17WASP which additionally facilities RPA loading onto ssDNA.