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.
Highlights
An ability to maintain genome integrity when threatened by adverse events occurring in the intracellular or extracellular environment is a biologically important trait that has been conserved among plants, animals, bacteria, and Archaea [1,2]
This reporter construct was introduced into a strain carrying a chromosomal rne insertion mutation that was complemented to viability by expression of a plasmid-borne gene producing either full length ribonuclease E (RNase E) or RNase G ([20,21], see Figure 1 legend) under control of a IPTG-regulated lac promoter
N was induced by addition of 0.1 mg/ml of mitomycin C (MTC). b-galactosidase activity was measured in SC5083 E. coli cells grown in the presence of 0.042 mM IPTG
Summary
An ability to maintain genome integrity when threatened by adverse events occurring in the intracellular or extracellular environment is a biologically important trait that has been conserved among plants, animals, bacteria, and Archaea [1,2]. Bacteria commonly react to the specific threat of DNA damage by mounting the SOS response, which assists the restoration of genome integrity and allows survival of DNA-damaged cells [3]. A prolonged SOS response may have a fitness cost [8] and the products of several genes are known to suppress SOS during normal cell growth and/or to have a role in its termination [9].
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