Arp2/3 and type-I myosins control chromosome mobility and end-resection at double-strand breaks in S. cerevisiae.

Using budding yeast, we show that 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 that is correlated with an increase in DSB mobility and DSB repair.
Mesh Terms:
Actin-Related Protein 2-3 Complex, Chromosomes, Fungal, DNA Breaks, Double-Stranded, DNA Helicases, DNA Repair, Endodeoxyribonucleases, Exodeoxyribonucleases, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins
Nat Commun
Date: Aug. 05, 2025
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