Ireton K, Grossman A D
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
J Bacteriol. 1992 May;174(10):3185-95. doi: 10.1128/jb.174.10.3185-3195.1992.
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, sigma K, at intermediate times during sporulation. The ski4 mutation caused the premature expression of cotA, a gene controlled by sigma K. An independent mutation that causes the premature activation of sigma 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 sigma K. Expression of ski4 was shown to be controlled by the sporulation-specific sigma factor sigma E.
枯草芽孢杆菌中的ski4::Tn917lac插入突变是在一次筛选中分离得到的，该筛选针对的是那些导致芽孢形成缺陷但被kinA（spoIIJ）编码的组氨酸蛋白激酶的存在或过表达所抑制的突变。ski4::Tn917lac在芽孢形成中造成了一个小缺陷，但与kinA的无效突变相结合时，会导致更严重的缺陷。插入突变位于一个87个氨基酸的开放阅读框（orf87，即bofA）中，该开放阅读框在芽孢形成的中间阶段控制一个σ因子σK的激活。ski4突变导致了cotA的过早表达，cotA是一个受σK控制的基因。一个导致σK过早激活的独立突变与kinA的无效突变相结合时，也导致了合成（协同）芽孢形成表型，这表明该缺陷是由于σK指导的基因表达时间改变所致。研究表明，ski4的表达受芽孢形成特异性σ因子σE的控制。
