OxyS small RNA induces cell cycle arrest to allow DNA damage repair.
Shir BarshishatMaya Elgrably-WeissJonathan EdelsteinJens GeorgSutharsan GovindarajanMeytal HavivPatrick R WrightWolfgang R HessShoshy AltuviaPublished in: The EMBO journal (2017)
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.
Keyphrases
- dna damage
- oxidative stress
- cell cycle arrest
- diabetic rats
- dna repair
- cell death
- dna damage response
- pi k akt
- escherichia coli
- transcription factor
- high glucose
- cell cycle
- single cell
- poor prognosis
- binding protein
- genome wide
- induced apoptosis
- gene expression
- amino acid
- signaling pathway
- drug induced
- stress induced
- mesenchymal stem cells
- single molecule
- pseudomonas aeruginosa
- small molecule
- long non coding rna
- klebsiella pneumoniae
- staphylococcus aureus
- multidrug resistant
- cystic fibrosis
- biofilm formation