Stressosomes formed in Bacillus subtilis from the RsbR protein of Listeria monocytogenes allow σ(B) activation following exposure to either physical or nutritional stress.

The general stress regulon of Bacillus subtilis is controlled by σ(B), a transcription factor that is activated by physical or nutritional stress. In B. subtilis, each of these two stresses is communicated to the primary σ(B) regulators by distinct pathways. Physical stress activation of σ(B) involves a large-molecular-mass (>10(6)-Da) structure (stressosome) formed by one or more homologous proteins (RsbRA, -B, -C, and -D) onto which the pathway's principal regulators are bound. The RsbR proteins are thought to be potential receptors for stress signaling. Listeria monocytogenes encodes orthologs of σ(B) and its principal regulators; however, unlike B. subtilis, L. monocytogenes appears to use the stressosome pathway for both physical and nutritional stress activation of σ(B). In the current work, a B. subtilis strain that expressed L. monocytogenes rsbR (rsbR(Lm)) in lieu of B. subtilis rsbR (rsbR(Bs)) was created and was found to display the Listeria phenotype of σ(B) activation following exposure to either physical or nutritional stress. B. subtilis expressing either the RsbR paralog rsbRC or rsbRD, but not rsbRA or rsbRB, as the sole source of RsbR also allowed σ(B) induction following nutritional stress. It is unclear whether the nutritional stress induction seen in these strains is the result of a direct effect of nutritional stress on stressosome activity or a consequence of the background levels of σ(B) activation in these strains and the effects of diminished ATP on the downstream phosphorylation reaction needed to reinactivate σ(B).