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EMBO J. 2018 Feb 1;37(3):413-426. doi: 10.15252/embj.201797651. Epub 2017 Dec 13.

OxyS small RNA induces cell cycle arrest to allow DNA damage repair.

Author information

1
Department of Microbiology and Molecular Genetics, IMRIC, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
2
Faculty of Biology, Genetics and Experimental Bioinformatics, University of Freiburg, Freiburg, Germany.
3
Bioinformatics Group, Department of Computer Science, University of Freiburg, Freiburg, Germany.
4
Faculty of Biology, Genetics and Experimental Bioinformatics, University of Freiburg, Freiburg, Germany wolfgang.hess@biologie.uni-freiburg.de shoshy.altuvia@mail.huji.ac.il.
5
Department of Microbiology and Molecular Genetics, IMRIC, The Hebrew University-Hadassah Medical School, Jerusalem, Israel wolfgang.hess@biologie.uni-freiburg.de shoshy.altuvia@mail.huji.ac.il.

Abstract

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.

KEYWORDS:

Escherichia coli ; cell cycle arrest; checkpoint; prophage; small RNA

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