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The facultative anaerobe,  Bacillus cereus , causes diarrheal diseases in humans. Its ability to deal with oxygen availability is recognized to be critical for pathogenesis. The  B. cereus  genome comprises a gene encoding a protein with high similarities to the redox regulator, Rex, which is a central regulator of anaerobic metabolism in  Bacillus subtilis  and other Gram-positive bacteria. Here, we showed that  B. cereus rex  is monocistronic and down-regulated in the absence of oxygen. The protein encoded by  rex  is an authentic Rex transcriptional factor since its DNA binding activity depends on the NADH/NAD +  ratio.  Rex  deletion compromised the ability of  B. cereus  to cope with external oxidative stress under anaerobiosis while increasing  B. cereus  resistance against such stress under aerobiosis. The deletion of  rex  affects anaerobic fermentative and aerobic respiratory metabolism of  B. cereus  by decreasing and increasing, respectively, the carbon flux through the NADH-recycling lactate pathway. We compared both the cellular proteome and exoproteome of the wild-type and Δ rex  cells using a high throughput shotgun label-free quantitation approach and identified proteins that are under control of Rex-mediated regulation. Proteomics data have been deposited to the ProteomeXchange with identifier PXD000886. The data suggest that Rex regulates both the cross-talk between metabolic pathways that produce NADH and NADPH and toxinogenesis, especially in oxic conditions.

Proteomic Evidences for Rex Regulation of Metabolism in Toxin-Producing Bacillus cereus ATCC 14579