A Novel Factor Controlling Bistability in Bacillus subtilis: the YmdB Protein Affects Flagellin Expression and Biofilm Formation
A Novel Factor Controlling Bistability in Bacillus subtilis: the YmdB Protein Affects Flagellin Expression and Biofilm Formation
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DOI：
10.1128/jb.05360-11
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发表时间：
2011-11-01
影响因子：
3.2
通讯作者：
Stuelke, Joerg
中科院分区：
文献类型：
--
作者：
Diethmaier, Christine;Pietack, Nico;Stuelke, Joerg
枯草芽孢杆菌的细胞可以是运动的或固着的，这取决于分别为鞭毛或生物膜形成所需的互斥基因组的表达。这两项活动都由主调节器SinR协调。我们已经分析了先前未表征的ymdB基因在B中的作用。枯草杆菌。我们在ymdB突变体中观察到编码鞭毛蛋白的hag基因和sigma（D）依赖性运动调节子的其他基因的强烈过表达，而用于生物膜形成的两个主要操纵子tapA-sipW-tasA和epsA-O不表达。因此，ymdB突变体不能形成生物膜。对群体中单个细胞的分析显示，ymdB突变体不再表现出痉挛行为;相反，所有细胞都是短的和能动的。ymdB突变体形成生物膜的能力受到抑制的sinR基因编码的生物膜形成的主调节器的删除，表明SinR依赖的抑制生物膜基因不能在ymdB突变体中被解除。我们的研究表明，缺乏表达的SlrR，SinR的拮抗剂，是负责观察到的表型。SlrR的过表达抑制ymdB突变的影响。
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 sigma(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.