Interactions among mutations that cause altered timing of gene expression during sporulation in Bacillus subtilis

Abstract

The ski4::Tn917lac insertion mutation in Bacillus subtilis was isolated in a screen for mutations that cause a defect in sporulation but that are suppressed by the presence or overexpression of the histidine protein kinase encoded by kinA (spoIIJ). ski4::Tn917lac caused a small defect in sporulation, but in combination with a null mutation in kinA, it caused a much more severe defect. The insertion mutation was in an 87-amino-acid open reading frame (orf87 bofA) that controls the activation of a sigma factor, σ(K), at intermediate times during sporulation. The ski4 mutation caused the premature expression of cotA, a gene controlled by σ(K). An independent mutation that causes the premature activation of σ(K) also caused a synthetic (synergistic) sporulation phenotype in combination with a null mutation in kinA, indicating that the defect was due to altered timing of gene expression directed by σ(K). Expression of ski4 was shown to be controlled by the sporulation-specific sigma factor σ(E).