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Stress-inducible mutagenesis mechanisms may provide important models for mutagenesis that drives host-pathogen interactions, antibiotic resistance, and possibly much of evolution generally. In\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Escherichia coli<\/jats:named-content>\n            , repair of DNA double-strand breaks is switched to a mutagenic mode, using error-prone DNA polymerases, via the SOS DNA damage and general (\u03c3\n            <jats:sup>S<\/jats:sup>\n            ) stress responses. We investigated small RNA (sRNA) clients of Hfq, an RNA chaperone that promotes mutagenic break repair (MBR), and found that GcvB promotes MBR by allowing a robust \u03c3\n            <jats:sup>S<\/jats:sup>\n            response, achieved via opposing the membrane stress (\u03c3\n            <jats:sup>E<\/jats:sup>\n            ) response. Cells that lack\n            <jats:italic>gcvB<\/jats:italic>\n            were MBR deficient and displayed reduced \u03c3\n            <jats:sup>S<\/jats:sup>\n            -dependent transcription but not reduced \u03c3\n            <jats:sup>S<\/jats:sup>\n            protein levels. The defects in MBR and \u03c3\n            <jats:sup>S<\/jats:sup>\n            -dependent transcription in \u0394\n            <jats:italic>gcvB<\/jats:italic>\n            cells were alleviated by artificially increasing \u03c3\n            <jats:sup>S<\/jats:sup>\n            levels, implying that GcvB promotes mutagenesis by allowing a normal \u03c3\n            <jats:sup>S<\/jats:sup>\n            response. \u0394\n            <jats:italic>gcvB<\/jats:italic>\n            cells were highly induced for the \u03c3\n            <jats:sup>E<\/jats:sup>\n            response, and blocking \u03c3\n            <jats:sup>E<\/jats:sup>\n            response induction restored both mutagenesis and \u03c3\n            <jats:sup>S<\/jats:sup>\n            -promoted transcription. We suggest that GcvB may promote the \u03c3\n            <jats:sup>S<\/jats:sup>\n            response and mutagenesis indirectly, by promoting membrane integrity, which keeps \u03c3\n            <jats:sup>E<\/jats:sup>\n            levels lower. At high levels, \u03c3\n            <jats:sup>E<\/jats:sup>\n            might outcompete \u03c3\n            <jats:sup>S<\/jats:sup>\n            for binding RNA polymerase and so reduce the \u03c3\n            <jats:sup>S<\/jats:sup>\n            response and mutagenesis. The data show the delicate balance of stress response modulation of mutagenesis.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            Mutagenesis mechanisms upregulated by stress responses promote\n            <jats:italic>de novo<\/jats:italic>\n            antibiotic resistance and cross-resistance in bacteria, antifungal drug resistance in yeasts, and genome instability in cancer cells under hypoxic stress. This paper describes the role of a small RNA (sRNA) in promoting a stress-inducible-mutagenesis mechanism, mutagenic DNA break repair in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Escherichia coli<\/jats:named-content>\n            . The roles of many sRNAs in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">E. coli<\/jats:named-content>\n            remain unknown. This study shows that \u0394\n            <jats:italic>gcvB<\/jats:italic>\n            cells, which lack the GcvB sRNA, display a hyperactivated membrane stress response and reduced general stress response, possibly because of sigma factor competition for RNA polymerase. This results in a mutagenic break repair defect. The data illuminate a function of GcvB sRNA in opposing the membrane stress response, and thus indirectly upregulating mutagenesis.\n          <\/jats:p>","DOI":"10.1128\/jb.00555-16","type":"journal-article","created":{"date-parts":[[2016,10,4]],"date-time":"2016-10-04T02:48:06Z","timestamp":1475549286000},"page":"3296-3308","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":20,"title":["The Small RNA GcvB Promotes Mutagenic Break Repair by Opposing the Membrane Stress Response"],"prefix":"10.1128","volume":"198","author":[{"given":"Brittany","family":"Barreto","sequence":"first","affiliation":[{"name":"Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA"},{"name":"Dan L. 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