Mueller J P, Sonenshein A L
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111.
J Bacteriol. 1992 Jul;174(13):4374-83. doi: 10.1128/jb.174.13.4374-4383.1992.
The Bacillus subtilis gsiA operon was induced rapidly, but transiently, as cells entered the stationary phase in nutrient broth medium. A mutation at the gsiC locus caused sporulation to be defective and expression of gsiA to be elevated and prolonged. The sporulation defect in this strain was apparently due to persistent expression of gsiA, since a gsiA null mutation restored sporulation to wild-type levels. Detailed mapping experiments revealed that the gsiC82 mutation lies within the kinA gene, which encodes the histidine protein kinase member of a two-component regulatory system. Since mutations in this gene caused a substantial blockage in expression of spoIIA, spoIIG, and spoIID genes, it seems that accumulation of a product of the gsiA operon interferes with sporulation by blocking the completion of stage II. It apparently does so by inhibiting or counteracting the activity of KinA.
当枯草芽孢杆菌在营养肉汤培养基中进入稳定期时，gsiA操纵子会迅速但短暂地被诱导。gsiC位点的突变导致芽孢形成缺陷，且gsiA的表达升高并延长。该菌株中的芽孢形成缺陷显然是由于gsiA的持续表达，因为gsiA基因缺失突变可将芽孢形成恢复到野生型水平。详细的定位实验表明，gsiC82突变位于kinA基因内，该基因编码双组分调节系统的组氨酸蛋白激酶成员。由于该基因的突变导致spoIIA、spoIIG和spoIID基因的表达严重受阻，似乎gsiA操纵子产物的积累通过阻止II期的完成来干扰芽孢形成。它显然是通过抑制或抵消KinA的活性来做到这一点的。
