Actin-Related Protein 6 (Arp6) Influences Double-Strand Break Repair in Yeast

DNA double-strand breaks (DSBs) are the most deleterious form of damage and repaired through non-homologous end-joining (NHEJ) or homologous recombination (HR). Repair initiation, regulation communication with signaling pathways require several histone-modifying chromatin-remodeling complexes. In budding yeast, this involves three primary complexes: INO80-C, which is primarily associated HR, SWR1-C, promotes NHEJ, RSC-C, involved in both as well general response. Here we identify ARP6 a factor DSB repair an RSC-C-related pathway. The loss significantly reduces NHEJ efficiency linearized plasmids cohesive ends, impairs chromosomal breaks, sensitizes cells to DNA-damaging agents. Genetic interaction analysis indicates that ARP6, MRE11 RSC-C function within same pathway, overexpression rescues rsc2∆ mre11∆ sensitivity Double mutants members INO80 SWR1 complexes, cause significant reduction efficiency, suggesting functions independently SWR1-C INO80-C. These findings support novel role for independent chromatin remodeling complex, apparent MRE11-associated