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鼠伤寒沙门氏菌鞭毛调节子中的一种新型转录调控机制:一种抗σ因子抑制鞭毛特异性σ因子σF的活性。

A novel transcriptional regulation mechanism in the flagellar regulon of Salmonella typhimurium: an antisigma factor inhibits the activity of the flagellum-specific sigma factor, sigma F.

作者信息

Ohnishi K, Kutsukake K, Suzuki H, Lino T

机构信息

Advanced Research Centre for Human Sciences, Waseda University, Saitama, Japan.

出版信息

Mol Microbiol. 1992 Nov;6(21):3149-57. doi: 10.1111/j.1365-2958.1992.tb01771.x.

DOI:10.1111/j.1365-2958.1992.tb01771.x
PMID:1453955
Abstract

We have studied the molecular mechanism of the negative regulation by flgM of the late operons of the flagellar regulon of Salmonella typhimurium. A 7.8 kDa protein that was identified as the flgM gene product was purified to homogeneity; its amino-terminal sequence was identical to the deduced sequence except for the lack of the initiating methionine. The purified FlgM repressed transcription from the fliC promoter, one that is activated by the sigma factor, FliA (sigma F). No DNA-binding activity was detected in FlgM. Chemical cross-linking experiments showed that the purified FlgM bound to sigma F and disturbed its ability to form a complex with RNA polymerase core enzyme. These results indicate that FlgM is a novel type of negative regulator that probably inactivates the flagellum-specific sigma factor through direct interaction, i.e. it is an anti-sigma factor.

摘要

我们研究了鼠伤寒沙门氏菌鞭毛调节子晚期操纵子flgM负调控的分子机制。一种被鉴定为flgM基因产物的7.8 kDa蛋白质被纯化至同质;其氨基末端序列与推导序列相同,只是缺少起始甲硫氨酸。纯化的FlgM抑制了fliC启动子的转录,fliC启动子由σ因子FliA(σF)激活。在FlgM中未检测到DNA结合活性。化学交联实验表明,纯化的FlgM与σF结合,并干扰其与RNA聚合酶核心酶形成复合物的能力。这些结果表明,FlgM是一种新型的负调控因子,可能通过直接相互作用使鞭毛特异性σ因子失活,即它是一种抗σ因子。

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