Oxidative stress is the main mechanism behind efficient disinfectants, causing damage in bacterial macromolecules. Importantly, bacteria activate resistance mechanisms in response to damage generated by oxidative stress. Strategies allowing pathogens to survive oxidative stress are highly conserved among microorganisms. Many of these strategies entail genomic responses triggered by signals transduced through Two Component Systems (TCS). Recently, we demonstrated that the TCS ArcAB (specifically ArcA) participates in bacterial responses to hypochlorite, regulating the uptake of this toxic compound and being involved in resistance and survival inside neutrophils, where hypochlorous acid abounds. Here, we demonstrated that ArcA is required in the response to oxidative stress generated by hypochlorite, independent of its cognate sensor ArcB or the Asp54 of ArcA, the only phosphorylable residue in ArcA, which is required to function as a gene regulator. Our results suggest that ArcA could have additional functions to respond to oxidative stress, independent of its regulatory activity, which might require interaction with other unknown relevant proteins.

氧化应激是有效消毒剂背后的主要机制，会导致细菌大分子损坏。重要的是，细菌响应于氧化应激产生的损害而激活抗性机制。微生物中高度保守病原体抵抗氧化应激的策略。这些策略中的许多策略都需要通过两组分系统（TCS）转换的信号触发基因组响应。最近，我们证明了TCS ArcAB（特别是ArcA）参与了对次氯酸盐的细菌反应，调节了该有毒化合物的摄取，并参与了次氯酸大量存在的嗜中性粒细胞的抵抗和生存。在这里，我们证明了在对次氯酸盐产生的氧化应激的反应中需要ArcA，与其关联传感器ArcB或ArcA的Asp54无关，ArcA中唯一的可磷酸化残基必须用作基因调节剂。我们的结果表明，ArcA可能具有其他功能来响应氧化应激，而与其调节活性无关，这可能需要与其他未知相关蛋白相互作用。