Isolation and Characterization of Bacillus subtilis sigB Operon Mutations That Suppress the Loss of the Negative Regulator RsbX

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Abstract
ς B , a transcription factor that controls the Bacillus subtilis general stress response regulon, is activated by either a drop in intracellular ATP or exposure to environmental stress. RsbX, one of seven ς B regulators (Rsb proteins) whose genes are cotranscribed with ς B , is a negative regulator in the stress-dependent activation pathway. To better define the interactions that take place among the Rsb proteins, we analyzed sigB operon mutations which suppress the high-level ς B activity that normally accompanies the loss of RsbX. Each of these mutations was in one of three genes ( rsbT , - U , and - V ) which encode positive regulators of ς B , and they all defined amino acid changes which either compromised the activities of the mutant Rsbs or affected their ability to accumulate. ς B activity remained inducible by ethanol in several of the RsbX − suppressor strains. This finding supports the notion that RsbX is not needed as the target for ς B activation by at least some stresses. ς B activity in several RsbX − strains with suppressor mutations in rsbT or - U was high during growth and underwent a continued, rather than a transient, increase following stress. Thus, RsbX is likely responsible for maintaining low ς B activity during balanced growth and for reestablishing ς B activity at prestress levels following induction. Although RsbX likely participates in limiting the ς B induction response, a second mechanism for curtailing unrestricted ς B activation was suggested by the ς B induction profile in two suppressor strains with mutations in rsbV . ς B activity in these mutants was stress inducible but transient, even in the absence of RsbX.