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一种控制枯草芽孢杆菌双稳定性的新型因子:YmdB 蛋白影响菌毛表达和生物膜形成。

A novel factor controlling bistability in Bacillus subtilis: the YmdB protein affects flagellin expression and biofilm formation.

机构信息

Department of General Microbiology, Georg August University Göttingen, Grisebachstr. 8, 37077 Göttingen, Germany.

出版信息

J Bacteriol. 2011 Nov;193(21):5997-6007. doi: 10.1128/JB.05360-11. Epub 2011 Aug 19.

Abstract

Cells of Bacillus subtilis can either be motile or sessile, depending on the expression of mutually exclusive sets of genes that are required for flagellum or biofilm formation, respectively. Both activities are coordinated by the master regulator SinR. We have analyzed the role of the previously uncharacterized ymdB gene for bistable gene expression in B. subtilis. We observed a strong overexpression of the hag gene encoding flagellin and of other genes of the σ(D)-dependent motility regulon in the ymdB mutant, whereas the two major operons for biofilm formation, tapA-sipW-tasA and epsA-O, were not expressed. As a result, the ymdB mutant is unable to form biofilms. An analysis of the individual cells of a population revealed that the ymdB mutant no longer exhibited bistable behavior; instead, all cells are short and motile. The inability of the ymdB mutant to form biofilms is suppressed by the deletion of the sinR gene encoding the master regulator of biofilm formation, indicating that SinR-dependent repression of biofilm genes cannot be relieved in a ymdB mutant. Our studies demonstrate that lack of expression of SlrR, an antagonist of SinR, is responsible for the observed phenotypes. Overexpression of SlrR suppresses the effects of a ymdB mutation.

摘要

枯草芽孢杆菌的细胞可以是运动的,也可以是静止的,这取决于分别用于鞭毛或生物膜形成的相互排斥的基因集的表达。这两种活性都由主调控因子 SinR 协调。我们分析了以前未表征的 ymdB 基因在枯草芽孢杆菌中双稳态基因表达的作用。我们观察到 ymdB 突变体中 hag 基因(编码鞭毛蛋白)和其他 σ(D)-依赖性运动调节子基因的强烈过表达,而生物膜形成的两个主要操纵子 tapA-sipW-tasA 和 epsA-O 则没有表达。结果,ymdB 突变体无法形成生物膜。对群体中单个细胞的分析表明,ymdB 突变体不再表现出双稳态行为;相反,所有细胞都是短而运动的。ymdB 突变体不能形成生物膜的能力被 sinR 基因缺失所抑制,sinR 基因编码生物膜形成的主调控因子,这表明 SinR 依赖性生物膜基因的抑制不能在 ymdB 突变体中得到缓解。我们的研究表明,SlrR(SinR 的拮抗剂)表达的缺失是导致观察到的表型的原因。SlrR 的过表达抑制了 ymdB 突变的影响。

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