Abstract
Following DNA double-strand breaks (DSBs) cells orchestrate a response that includes the activation of signaling pathways and repair of the damage. Posttranslational modifications (PTMs) of chromatin around the break site play a key role in this process. Ahmad et al. (e00056-21) characterized a novel DNA damage-induced histone phosphorylation, on H2A serine 15 in Saccharomyces cerevisiae. They showed that this modification depends on Mec1ATR and functions to increase the resection of DNA ends, most likely through a mechanism involving the regulation of Rad953BP1. This study highlights an evolutionally conserved function for PTMs at a specific location on the H2A N-terminal tail in the regulation of DSBs repair pathway choice.