摘要：In many bacteria, OxyR is the major regulator controlling cellular response to H2O2. A common phenotype resulting from OxyR loss is reduced growth rate, but the underlying mechanism is unknown. We demonstrated in Shewanella oneidensis, an important research model for applied and environmental microbes, that the defect is primarily due to an electron shortage to major terminal oxidase cytochrome cbb3. The loss of OxyR leads to enhanced production of electron carriers that compete for electrons against cytochrome cbb3, cytochrome bd in particular. We further showed that the oxyR mutation also results in increased production of menaquinone, an additional means to lessen electrons to cytochrome cbb3. Although regulation of OxyR on these biological processes appears to be indirect, these data indicate that the regulator plays a previously underappreciated role in mediating respiration.
