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枯草芽孢杆菌芽孢形成过程中孢子光产物裂解酶操纵子(splAB)的调控:P1启动子突变和splA的框内缺失对splB-lacZ融合表达的调节

Spore photoproduct lyase operon (splAB) regulation during Bacillus subtilis sporulation: modulation of splB-lacZ fusion expression by P1 promoter mutations and by an in-frame deletion of splA.

作者信息

Pedraza-Reyes M, Gutiérrez-Corona F, Nicholson W L

机构信息

Instituto de Investigacion en Biología Experimental, Facultad de Química, Universidad de Guanajuato, Guanajuato, Gto., Mexico.

出版信息

Curr Microbiol. 1997 Mar;34(3):133-7. doi: 10.1007/s002849900157.

DOI:10.1007/s002849900157
PMID:9009064
Abstract

EsigmaG-dependent transcription of the splAB operon in the forespore at stage III of Bacillus subtilis sporulation initiates from two promoters, P1 preceding splA (major) and P3 preceding splB (minor). To explore the possible role of splA in controlling splB-encoded spore photoproduct lyase expression, we measured beta-galactosidase from splB-lacZ fusions integrated at the SPbeta prophage locus which contained point mutations or deletions which either inactivated or physically removed P1 and/or splA. Paradoxically, inactivation of P1 by point mutation or its removal by deletion from upstream resulted in elevated beta-galactosidase expression of the resulting splB-lacZ fusion, as did an in-frame deletion of splA which left P1 and P3 intact;however, expression of all fusions remained sporulation specific and EsigmaG dependent.

摘要

枯草芽孢杆菌芽孢形成III期前芽孢中,splAB操纵子的σG依赖性转录起始于两个启动子,即位于splA之前的P1(主要)和位于splB之前的P3(次要)。为了探究splA在控制splB编码的芽孢光产物裂解酶表达中可能发挥的作用,我们测定了整合在SPβ原噬菌体位点的splB - lacZ融合基因的β-半乳糖苷酶活性,这些融合基因含有点突变或缺失,这些突变或缺失会使P1失活或从上游物理去除P1和/或splA。矛盾的是,通过点突变使P1失活或从上游删除P1都会导致所得splB - lacZ融合基因的β-半乳糖苷酶表达升高,与使P1和P3保持完整的splA框内缺失的情况相同;然而,所有融合基因的表达仍具有芽孢形成特异性且依赖于σG。

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