Biology Department, Gonzaga University, Spokane, Washington.
J Basic Microbiol. 2019 Aug;59(8):834-845. doi: 10.1002/jobm.201900076. Epub 2019 Jun 18.
A bacterium's ability to thrive in the presence of multiple environmental stressors simultaneously determines its resilience. We showed that activation of the SigB-controlled general stress response by mild environmental or energy stress provided significant cross-protection to subsequent lethal oxidative, disulfide and nitrosative stress in Bacillus subtilis. SigB activation is mediated via the stressosome and RsbP, the main conduits of environmental and energy stress, respectively. Cells exposed to mild environmental stress while lacking the major stressosome components RsbT or RsbRA were highly sensitive to subsequent oxidative stress, whereas rsbRB, rsbRC, rsbRD, and ytvA null mutants showed a spectrum of sensitivity, confirming their redundant roles and suggesting they could modulate the signals generated by environmental or oxidative stress. By contrast, cells encountering stationary phase stress required RsbP but not RsbT to survive subsequent oxidative stress. Interestingly, optimum cross-protection against nitrosative stress caused by sodium nitropruside required SigB but not the known regulators, RsbT and RsbP, suggesting an additional and as yet uncharacterized route of SigB activation independent of the known regulators. Together, these results provide mechanistic information on how B. subtilis promotes enhanced resistance against lethal oxidative stress during mild environmental and energy stress conditions.
一种细菌在同时存在多种环境胁迫的情况下茁壮成长的能力决定了它的弹性。我们表明,轻度环境或能源胁迫引发 SigB 控制的一般应激反应,为随后枯草芽孢杆菌的致命氧化、二硫键和硝化应激提供了显著的交叉保护。SigB 的激活是通过应激体和 RsbP 介导的,应激体和 RsbP 分别是环境和能源应激的主要通道。当细胞暴露在缺乏主要应激体成分 RsbT 或 RsbRA 的轻度环境胁迫下时,对随后的氧化应激高度敏感,而 rsbRB、rsbRC、rsbRD 和 ytvA 缺失突变体表现出一系列的敏感性,这证实了它们的冗余作用,并表明它们可以调节环境或氧化应激产生的信号。相比之下,遇到静止期应激的细胞需要 RsbP 但不需要 RsbT 来在随后的氧化应激中存活。有趣的是,最优的硝普酸钠引起的硝化应激交叉保护需要 SigB,但不需要已知的调节因子 RsbT 和 RsbP,这表明 SigB 的激活有一个额外的、尚未被描述的途径,独立于已知的调节因子。总之,这些结果提供了枯草芽孢杆菌在轻度环境和能源胁迫条件下促进增强抵抗致命氧化应激的机制信息。