Abstract
Using budding yeast, we show that the Arp2/3 actin branching complex has
an evolutionarily conserved role in promoting chromosome mobility of
double-strand breaks (DSBs). The radius of confinement of a broken
chromosome is reduced by inhibiting Arp2/3 or by auxin-induced degron
depletion of the nucleation-promoting factor Las17WASP or type-1 myosins.
Arp2/3 and Las17 are required both to initiate and maintain 5 ' to
3' resection of DSB ends, whereas depleting Myo3 or Myo5 impairs
broken chromosome motion without affecting resection. Conversely,
inhibiting Exo1- and Dna2-dependent long-range resection reduces DSB
mobility. Inactivating Arp2/3 before DSB induction leads to shortened
checkpoint arrest, activating the Tel1ATM/Mre11 (TM) checkpoint. Shortened
checkpoint arrest, but not reduced broken chromosome mobility per se,
results in reduced interchromosomal homologous recombination. These
results suggest that regulating the Arp2/3 complex plays a key role in the
processing of DSB ends, which is correlated with an increase in DSB
mobility and DSB repair.