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Humans are inextricably linked to each other and our natural world, and microorganisms lie at the nexus of those interactions. Microorganisms form genetically flexible, taxonomically diverse, and biochemically rich communities, i.e., microbiomes that are integral to the health and development of macroorganisms, societies, and ecosystems. Yet engagement with beneficial microbiomes is dictated by access to public resources, such as nutritious food, clean water and air, safe shelter, social interactions, and effective medicine. In this way, microbiomes have sociopolitical contexts that must be considered. The Microbes and Social Equity (MSE) Working Group connects microbiology with social equity research, education, policy, and practice to understand the interplay of microorganisms, individuals, societies, and ecosystems. Here, we outline opportunities for integrating microbiology and social equity work through broadening education and training; diversifying research topics, methods, and perspectives; and advocating for evidence-based public policy that supports sustainable, equitable, and microbial wealth for all.

The ability to monitor the environment for toxic chemical and physical disturbances is essential for bacteria that live in dynamic environments. The fundamental sensing mechanisms and physiological responses that allow bacteria to thrive are conserved even if the molecular components of these pathways are not. The bacterial general stress response (GSR) represents a conceptual model for how one pathway integrates a wide range of environmental signals, and how a generalized system with broad molecular responses is coordinated to promote survival likely through complementary pathways. Environmental stress signals such as heat, osmotic stress, and pH changes are received by sensor proteins that through a signaling cascade activate the sigma factor, SigB, to regulate over 200 genes. Additionally, the GSR plays an important role in stress priming that increases bacterial fitness to unrelated subsequent stressors such as oxidative compounds. While the GSR response is implicated during oxidative stress, the reason for its activation remains unknown and suggests crosstalk between environmental and oxidative stress sensors and responses to coordinate antioxidant functions. Systems levels studies of cellular responses such as transcriptomes, proteomes, and metabolomes of stressed bacteria and single-cell analysis could shed light into the regulated functions that protect, remediate, and minimize damage during dynamic environments. This perspective will focus on fundamental stress sensing mechanisms and responses in Gram-positive bacterial species to illustrate their commonalities at the molecular and physiological levels; summarize exciting directions; and highlight how system-level approaches can help us understand bacterial physiology.

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 nutritional stress provided significant cross-protection to subsequent lethal oxidative, disulfide and nitrosative stress exposure. SigB activation is mediated via the stressosome and RsbP, the main conduits of environmental and nutritional stress, respectively. Cells exposed to mild environmental stress while lacking the major stressosome components RsbT or RsbRA were highly sensitive to subsequent oxidative stress, whereasrsbRB, rsbRC, rsbRDandytvAnull mutants showed a spectrum of sensitivity, confirming their redundant roles and suggesting they could modulate the signal generated by environmental stress or oxidative stress. Furthermore, from mutant analysis we infer that RsbRA phosphorylation by RsbT was important for this cross-resistance to oxidative stress. By contrast, cells encountering stationary phase stress required RsbP but not RsbT to survive subsequent oxidative stress caused by hydrogen peroxide and diamide. Interestingly, optimum cross-protection against nitrosative stress caused by SNP 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 environmental and energy-stress pathways. Together, these results provide a mechanism for howBacillus subtilispromotes enhanced resistance against lethal oxidative stress during likely physiologically relevant conditions such as mild environmental or nutrient stress.