δ(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 δ(B) regulators (Rsb proteins) whose genes are cotranscribed with δ(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 δ(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 δ(B), and they all defined amino acid changes which either compromised the activities of the mutant Rsbs or affected their ability to accumulate. δ(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 δ(B) activation by at least some stresses. δ(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 δ(B) activity during balanced growth and for reestablishing δ(B) activity at prestress levels following induction. Although RsbX likely participates in limiting the δ(B) induction response, a second mechanism for curtailing unrestricted δ(B) activation was suggested by the δ(B) induction profile in two suppressor strains with mutations in rsbV, δ(B) activity in these mutants was stress inducible but transient, even in the absence of RsbX.
ASJC Scopus subject areas
- Molecular Biology