In 1993, Benson and Haldenwang investigated the σB-dependent promoter of the Bacillus subtilis sigB operon and its induction by heat shock. They found that σB, a secondary sigma factor, increased 5- to 10-fold when cultures were shifted from 37°C to 48°C. Western blot analyses showed that σB, RsbV, and RsbW increased coordinately after heat shock, with this increase dependent on σB but not RsbV. Nuclease protection experiments supported that the shift to 48°C enhanced transcription from the σB-dependent promoter of the sigB operon. The level of mRNA initiating at the σB-dependent ctc promoter also increased 5- to 10-fold after heat shock. Pulse-labeling showed that σB wild-type and mutant strains produced similar amounts of major heat-inducible proteins, but wild-type strains produced seven additional proteins not present in the σB null mutant. Although σB is not essential for essential heat shock genes, it is activated by heat shock to elevate its own synthesis and possibly other heat-inducible proteins. σB is a minor sigma factor in Bacillus subtilis, associated with RNA polymerase but disappearing during sporulation. It is a regulatory protein with an elaborate mechanism to control its activity. σB is part of a four-gene operon with rsbV, rsbW, and rsbX, involved in controlling σB activity. Previous studies suggested that these genes operate in a negative control pathway, with RsbW inhibiting σB activity. Mutations in RsbW severely impair growth and lead to suppressor mutations. Two genes, ctc and csbA, depend on σB for expression. Both are maximally expressed at the end of exponential growth in media that suppress sporulation and the tricarboxylic acid cycle. The roles of ctc and csbA are undefined, but neither is essential for growth or sporulation. The ctc null mutation results in temperature-sensitive oligosporangeny. In Escherichia coli, heat shock induces proteins encoded by a regulon transcribed by σ32. The temperature-sensitive phenotype of the ctc mutant suggested σB might be the B. subtilis counterpart of σ32, but this was not supported. B. subtilis strains with null mutations in sigB are not more temperature sensitive than wild-type strains, suggesting σB is not equivalent to σ32. σB is not essential for survival at elevated temperatures, indicating its role during heat shock is not critical. A monoclonal antibody against σB was used to monitor its levels in response to temperature increase. Western blot analysis showed σB is a heat-inducible protein, with levels rising rapidly when B. subtilis cultures are shifted from 37°C to 48°C. TheIn 1993, Benson and Haldenwang investigated the σB-dependent promoter of the Bacillus subtilis sigB operon and its induction by heat shock. They found that σB, a secondary sigma factor, increased 5- to 10-fold when cultures were shifted from 37°C to 48°C. Western blot analyses showed that σB, RsbV, and RsbW increased coordinately after heat shock, with this increase dependent on σB but not RsbV. Nuclease protection experiments supported that the shift to 48°C enhanced transcription from the σB-dependent promoter of the sigB operon. The level of mRNA initiating at the σB-dependent ctc promoter also increased 5- to 10-fold after heat shock. Pulse-labeling showed that σB wild-type and mutant strains produced similar amounts of major heat-inducible proteins, but wild-type strains produced seven additional proteins not present in the σB null mutant. Although σB is not essential for essential heat shock genes, it is activated by heat shock to elevate its own synthesis and possibly other heat-inducible proteins. σB is a minor sigma factor in Bacillus subtilis, associated with RNA polymerase but disappearing during sporulation. It is a regulatory protein with an elaborate mechanism to control its activity. σB is part of a four-gene operon with rsbV, rsbW, and rsbX, involved in controlling σB activity. Previous studies suggested that these genes operate in a negative control pathway, with RsbW inhibiting σB activity. Mutations in RsbW severely impair growth and lead to suppressor mutations. Two genes, ctc and csbA, depend on σB for expression. Both are maximally expressed at the end of exponential growth in media that suppress sporulation and the tricarboxylic acid cycle. The roles of ctc and csbA are undefined, but neither is essential for growth or sporulation. The ctc null mutation results in temperature-sensitive oligosporangeny. In Escherichia coli, heat shock induces proteins encoded by a regulon transcribed by σ32. The temperature-sensitive phenotype of the ctc mutant suggested σB might be the B. subtilis counterpart of σ32, but this was not supported. B. subtilis strains with null mutations in sigB are not more temperature sensitive than wild-type strains, suggesting σB is not equivalent to σ32. σB is not essential for survival at elevated temperatures, indicating its role during heat shock is not critical. A monoclonal antibody against σB was used to monitor its levels in response to temperature increase. Western blot analysis showed σB is a heat-inducible protein, with levels rising rapidly when B. subtilis cultures are shifted from 37°C to 48°C. The