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OxyS small RNA induces cell cycle arrest to allow DNA damage repair
Author(s) -
Barshishat Shir,
ElgrablyWeiss Maya,
Edelstein Jonathan,
Georg Jens,
Govindarajan Sutharsan,
Haviv Meytal,
Wright Patrick R,
Hess Wolfgang R,
Altuvia Shoshy
Publication year - 2017
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201797651
Subject(s) - dna damage , microbiology and biotechnology , cell cycle checkpoint , dna repair , biology , ftsz , transcription (linguistics) , g2 m dna damage checkpoint , sos response , dna , cell cycle , transcription factor , cell division , rna , cell , genetics , gene , linguistics , philosophy
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.