Louie P, Lee A, Stansmore K, Grant R, Ginther C, Leighton T
Department of Biochemistry and Molecular Biology, University of California, Berkeley 94720.
J Bacteriol. 1992 Jun;174(11):3570-6. doi: 10.1128/jb.174.11.3570-3576.1992.
Bacillus subtilis strains containing defects in the sporulation gene spoIIF (kinA), spoIIJ (kinA), or spoIIN (ftsA) cannot transcribe the sigma E-dependent gene spoIID. Results presented here and by other workers demonstrate that the spoIIF, spoIIJ, and spoIIN gene products control spoIID transcription indirectly by coordinating the induction of the spoIIGAB, spoIIE, and spoIIAC operons, which are required for sigma E synthesis and processing. Sporulation competence and spoIIGAB, spoIIE, and spoIIAC transcription were restored in spoIIF, spoIIJ, and spoIIN mutants by introduction of crsA47, a mutation in the major vegetative sigma factor sigma A. crsA mutations are known to restore sporulation in certain spo0 mutants. crsA suppression of kinA and ftsA mutations was achieved through inhibition of the transcription of sin, a gene involved in the selection between several post-exponential-phase cell states. A deletion of sin restored sporulation competence in spoIIF, spoIIJ, or spoIIN mutant strains. A sin deletion was also able to restore sporulation competence in the crsA suppressible stage 0 mutant spo0K141.
在芽孢形成基因spoIIF(kinA)、spoIIJ(kinA)或spoIIN(ftsA)中存在缺陷的枯草芽孢杆菌菌株无法转录依赖于σE的基因spoIID。本文及其他研究者展示的结果表明,spoIIF、spoIIJ和spoIIN基因产物通过协调spoIIGAB、spoIIE和spoIIAC操纵子的诱导来间接控制spoIID转录,而这些操纵子是σE合成和加工所必需的。通过引入主要营养型σ因子σA中的一个突变crsA47,spoIIF、spoIIJ和spoIIN突变体中的芽孢形成能力以及spoIIGAB、spoIIE和spoIIAC转录得以恢复。已知crsA突变可在某些spo0突变体中恢复芽孢形成。通过抑制sin(一个参与几种指数后期细胞状态选择的基因)的转录,实现了对kinA和ftsA突变的crsA抑制。sin缺失可恢复spoIIF、spoIIJ或spoIIN突变菌株中的芽孢形成能力。sin缺失也能够恢复crsA可抑制的0期突变体spo0K141中的芽孢形成能力。