{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T05:55:37Z","timestamp":1792648537094,"version":"4.5.0"},"reference-count":56,"publisher":"American Society for Microbiology","issue":"13","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Bacteriol."],"published-print":{"date-parts":[[2015,7,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Oxidative stresses triggered by reactive oxygen species (ROS) that damage various cellular components are unavoidable for virtually all living organisms. In defense, microorganisms have evolved sophisticated mechanisms to sense, respond to, and battle against ROS.<jats:named-content content-type=\"genus-species\">Shewanella oneidensis<\/jats:named-content>, an important research model for applied and environmental microbes, employs OxyR to mediate the response to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>by derepressing the production of the major H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>scavenger KatB as a major means toward these goals. Surprisingly, despite enhanced H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>degradation, the<jats:italic>oxyR<\/jats:italic>mutant carries a viability deficiency phenotype (plating defect), which can be suppressed by the addition of exogenous iron species. Experiments showed that the defect was not due to iron starvation. Rather, multiple lines of evidence suggested that H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>generated abiotically in lysogeny broth (LB) is responsible for the defect by quickly killing mutant cells. We then showed that the iron species suppressed the plating defect by two distinct mechanisms, either as an H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>scavenger without involving living cells or as an environmental cue to stimulate an OxyR-independent response to help cells cope with oxidative stress. Based on the suppression of the plating defect by overproduction of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>scavengers<jats:italic>in vivo<\/jats:italic>, we propose that cellular components that are vulnerable to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>and responsible for the defect may reside outside the cytoplasm.<\/jats:p><jats:p><jats:bold>IMPORTANCE<\/jats:bold>In bacteria, OxyR is the major regulator controlling the cellular response to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>. The loss of OxyR results in reduced viability in many species, but the underlying mechanism is unknown. We showed in<jats:named-content content-type=\"genus-species\">S. oneidensis<\/jats:named-content>that this defect was due to H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>generated abiotically in LB. We then showed that this defect could be corrected by the addition of Fe<jats:sup>2+<\/jats:sup>or catalase to the LB or increased intracellular production of catalase. Further analyses revealed that Fe<jats:sup>2+<\/jats:sup>was able not only to decompose H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>directly but also to stimulate the activity of OxyR-independent H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>-scavenging enzymes. Our data indicate that iron species play a previously underappreciated role in protecting cells from H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>in environments.<\/jats:p>","DOI":"10.1128\/jb.00154-15","type":"journal-article","created":{"date-parts":[[2015,4,21]],"date-time":"2015-04-21T02:22:22Z","timestamp":1429582942000},"page":"2179-2189","source":"Crossref","is-referenced-by-count":59,"title":["Unraveling the Mechanism for the Viability Deficiency of Shewanella oneidensis oxyR Null 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