Abstract
Oxidative stress is one of the major challenges that Shewanella encounter routinely because they thrive in redox-stratified environments prone to reactive oxygen species (ROS) formation, letting alone that ROS can be generated endogenously. As respiration is the predominant process for endogenous ROS, regulators mediating respiration have been demonstrated and/or implicated to play a role in oxidative stress response. In our efforts to unveil the involvement of global regulators for respiration in the oxidative stress response, we found that loss of the Arc system increases S. oneidensis sensitivity to H2O2 whereas neither Fnr nor Crp has a significant role. A comparison of transcriptomic profiles of the wild-type and its isogenic arcA mutant revealed that the OxyR regulon is independent of the Arc system. We then provided evidence that the enhanced H2O2 sensitivity of the arcA mutant is due to an increased H2O2 uptake rate, a result of a cell envelope defect. Although one of three proteases of the ArcA regulon when in excess is partially accountable for the envelope defect, the major contributors remain elusive. Overall, our data indicate that the Arc system influences the bacterial cell envelope biosynthesis, a physiological aspect that has not been associated with the regulator before.
Highlights
Conserved among Gram-negative and -positive bacteria, is specific for responding to organic peroxide (OP) [3]
Instead of the low density of cells used in determining MIC, H2O2 discs were applied to a bacterial cell lawn
As reactive oxygen species (ROS) can be formed intracellularly when molecular oxygen interacts with redox enzymes [54], global regulators for respiration, especially the Arc system, have been implicated in bacterial oxidative stress response
Summary
Conserved among Gram-negative and -positive bacteria, is specific for responding to organic peroxide (OP) [3]. Two redox-sensing global regulatory systems mediating the transition from aerobic to anaerobic metabolism, Fnr (fumarate and nitrate reduction regulator) and Arc (aerobic respiration control) two-component system, have been implicated to have an important role in the resistance to ROS-induced damage [6,7,8,9,10,11,12]. Unlike its counterpart in E. coli, this atypical system plays an important role in aerobic respiration without interfering with expression of genes encoding components of the tricarboxylic acid (TCA) cycle [28,29,30]. We showed that this defect is partially attributable to overproduction of SO1915, one of three proteases of the ArcA regulon It seems that the impaired envelope resulting from the arcA mutation is rather complex, unlikely depending on a single gene. The present study for the first time links the Arc system with the biosynthesis of bacterial cell envelope
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