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Ribonuclease E Modulation of the Bacterial SOS Response

Authors
Journal
PLoS ONE
1932-6203
Publisher
Public Library of Science
Publication Date
Volume
7
Issue
6
Identifiers
DOI: 10.1371/journal.pone.0038426
Keywords
  • Research Article
  • Biology
  • Biochemistry
  • Genetics
  • Gene Expression
  • Rna Processing
  • Rna Stability
  • Genetic Mutation
  • Molecular Genetics
  • Microbiology
  • Microbial Control
  • Microbial Mutation
  • Microbial Physiology
  • Molecular Cell Biology
  • Cellular Stress Responses
Disciplines
  • Biology
  • Ecology
  • Geography

Abstract

Plants, animals, bacteria, and Archaea all have evolved mechanisms to cope with environmental or cellular stress. Bacterial cells respond to the stress of DNA damage by activation of the SOS response, the canonical RecA/LexA-dependent signal transduction pathway that transcriptionally derepresses a multiplicity of genes–leading to transient arrest of cell division and initiation of DNA repair. Here we report the previously unsuspected role of E. coli endoribonuclease RNase E in regulation of the SOS response. We show that RNase E deletion or inactivation of temperature-sensitive RNase E protein precludes normal initiation of SOS. The ability of RNase E to regulate SOS is dynamic, as down regulation of RNase E following DNA damage by mitomycin C resulted in SOS termination and restoration of RNase E function leads to resumption of a previously aborted response. Overexpression of the RraA protein, which binds to the C-terminal region of RNase E and modulates the actions of degradosomes, recapitulated the effects of RNase E deficiency. Possible mechanisms for RNase E effects on SOS are discussed.

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