| Summary: | Oxidative stress resistance is an important mechanism to sustain the viability of oxygen-sensitive microaerophilic <i>Campylobacter jejuni</i>. In <i>C. jejuni</i>, gene expression associated with oxidative stress defense is modulated by PerR (peroxide response regulator) and CosR (<i>Campylobacter</i> oxidative stress regulator). Iron also plays an important role in the regulation of oxidative stress, as high iron concentrations reduce the transcription of <i>perR</i>. However, little is known about how iron affects the transcription of <i>cosR</i>. The level of <i>cosR</i> transcription was increased when the defined media MEMα (Minimum Essential Medium) was supplemented with ferrous (Fe<sup>2+</sup>) and ferric (Fe<sup>3+</sup>) iron and the Mueller–Hinton (MH) media was treated with an iron chelator, indicating that iron upregulates <i>cosR</i> transcription. However, other divalent cationic ions, such as Zn<sup>2+</sup>, Cu<sup>2+</sup>, Co<sup>2+</sup>, and Mn<sup>2+</sup>, did not affect <i>cosR</i> transcription, suggesting that <i>cosR</i> transcription is regulated specifically by iron. Interestingly, the level of <i>perR</i> transcription was increased when CosR was overexpressed. The positive regulation of <i>perR</i> transcription by CosR was observed both in the presence or in the absence of iron. The results of the electrophoretic mobility shift assay showed that CosR directly binds to the <i>perR</i> promoter. DNase I footprinting assays revealed that the CosR binding site in the <i>perR</i> promoter overlaps with the PerR box. In the study, we demonstrated that <i>cosR</i> transcription is increased in iron-rich conditions, and CosR positively regulates the transcription of PerR, another important regulator of oxidative stress defense in <i>C. jejuni</i>. These results provide new insight into how <i>C. jejuni</i> regulates oxidative stress defense by coordinating the transcription of <i>perR</i> and <i>cosR</i> in response to iron.
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