Caiazza Nicky C, Merritt Judith H, Brothers Kimberly M, O'Toole George A
Dept. of Microbiology & Immunology, Rm. 505, Vail Building, Dartmouth Medical School, Hanover, NH 03755, USA.
J Bacteriol. 2007 May;189(9):3603-12. doi: 10.1128/JB.01685-06. Epub 2007 Mar 2.
We previously reported that SadB, a protein of unknown function, is required for an early step in biofilm formation by the opportunistic pathogen Pseudomonas aeruginosa. Here we report that a mutation in sadB also results in increased swarming compared to the wild-type strain. Our data are consistent with a model in which SadB inversely regulates biofilm formation and swarming motility via its ability both to modulate flagellar reversals in a viscosity-dependent fashion and to influence the production of the Pel exopolysaccharide. We also show that SadB is required to properly modulate flagellar reversal rates via chemotaxis cluster IV (CheIV cluster). Mutational analyses of two components of the CheIV cluster, the methyl-accepting chemotaxis protein PilJ and the PilJ demethylase ChpB, support a model wherein this chemotaxis cluster participates in the inverse regulation of biofilm formation and swarming motility. Epistasis analysis indicates that SadB functions upstream of the CheIV cluster. We propose that P. aeruginosa utilizes a SadB-dependent, chemotaxis-like regulatory pathway to inversely regulate two key surface behaviors, biofilm formation and swarming motility.
我们之前报道过,SadB是一种功能未知的蛋白质,它是机会致病菌铜绿假单胞菌生物膜形成早期步骤所必需的。在此我们报道,与野生型菌株相比,sadB突变也会导致群体游动增加。我们的数据与一个模型相符,即SadB通过其以黏度依赖方式调节鞭毛反转以及影响Pel胞外多糖产生的能力,反向调节生物膜形成和群体游动。我们还表明,SadB需要通过趋化性IV簇(CheIV簇)来适当调节鞭毛反转速率。对CheIV簇的两个组分,即甲基接受趋化蛋白PilJ和PilJ去甲基化酶ChpB的突变分析,支持了这样一个模型,即该趋化簇参与生物膜形成和群体游动的反向调节。上位性分析表明,SadB在CheIV簇的上游起作用。我们提出,铜绿假单胞菌利用一种依赖SadB的、类似趋化性的调控途径来反向调节两种关键的表面行为,即生物膜形成和群体游动。