To maintain genome integrity, organisms employ DNA damage response, the underlying principles of which are conserved from bacteria to humans. The bacterial small RNA OxyS of Escherichia coli is induced upon oxidative stress and has been implicated in protecting cells from DNA damage; however, the mechanism by which OxyS confers genome stability remained unknown. Here, we revealed an OxyS-induced molecular checkpoint relay, leading to temporary cell cycle arrest to allow damage repair. By repressing the expression of the essential transcription termination factor nusG, OxyS enables read-through transcription into a cryptic prophage encoding kilR. The KilR protein interferes with the function of the major cell division protein FtsZ, thus imposing growth arrest. This transient growth inhibition facilitates DNA damage repair, enabling cellular recovery, thereby increasing viability following stress. The OxyS-mediated growth arrest represents a novel tier of defense, introducing a new regulatory concept into bacterial stress response.
Bibliographical noteFunding Information:
This work was supported by the German-Israeli Foundation (G-1311-416.13/ 2015); the Israel Science Foundation founded by The Israel Academy of Sciences and Humanities (711/13); the Israel Centers of Research Excellence (ICORE), Chromatin and RNA (1796/12); the German Federal Ministry for Education and Research (BMBF) program de.NBI-Partner (Grant 031L0106B) and Deutsch-Israelische Projektkooperation (AM 441/1-1 SO 568/1-1).
© 2017 The Authors. Published under the terms of the CC BY 4.0 license
- Escherichia coli
- cell cycle arrest
- small RNA