DNA double strand break end-processing and RecA induce RecN expression levels in Bacillus subtilis

• Bacillus subtilis RecN is among the first responders to DNA double strand breaks (DSBs).
• Two major signaling-related cascades (SOS and DSBR) are induced upon DSBs.
• Neither the absence of LexA or RecO nor the phosphorylation state of RecA or SsbA significantly affected RecN expression levels.
• End-processing functions and the RecA protein itself contribute to increase the RecN levels after DNA DSBs.
• DSBs activate a signal process that drives cellular responses SOS and DSBR in bacteria and ATM and ATR in eukaryotic cells.

Bacillus subtilis cells respond to double strand breaks (DSBs) with an ordered recruitment of repair proteins to the site lesion, being RecN one of the first responders. In B. subtilis, one of the responses to DSBs is to increase RecN expression rather than modifying its turnover rate. End-processing activities and the RecA protein itself contribute to increase RecN levels after DNA DSBs. RecO is required for RecA filament formation and full SOS induction, but its absence did not significantly affect RecN expression. Neither the absence of LexA nor the phosphorylation state of RecA or SsbA significantly affect RecN expression levels. These findings identify two major mechanisms (SOS and DSB response) used to respond to DSBs, with LexA required for one of them (SOS response). The DSB response, which requires end-processing and RecA or short RecO-independent RecA filaments, highlights the importance of guarding genome stability by modulating the DNA damage responses.