Belas R, Schneider R, Melch M
Center of Marine Biotechnology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21202, USA.
J Bacteriol. 1998 Dec;180(23):6126-39. doi: 10.1128/JB.180.23.6126-6139.1998.
Proteus mirabilis swarming behavior is characterized by the development of concentric rings of growth that are formed as cyclic events of swarmer cell differentiation, swarming migration, and cellular differentiation are repeated during colony translocation across a surface. This cycle produces the bull's-eye colony often associated with cultures of P. mirabilis. How the cells communicate with one another to coordinate these perfectly synchronized rings is presently unknown. We report here the identification of a genetic locus that, when mutated, results in a precocious swarming phenotype. These mutants are defective in the temporal control of swarming migration and start swarming ca. 60 min sooner than wild-type cells. Unlike the wild type, precocious swarming mutants are also constitutive swarmer cells and swarm on minimal agar medium. The defects were found to be localized to a 5.4-kb locus on the P. mirabilis genome encoding RsbA (regulator of swarming behavior) and the P. mirabilis homologs to RcsB and RcsC. RsbA is homologous to membrane sensor histidine kinases of the two-component family of regulatory proteins, suggesting that RsbA may function as a sensor of environmental conditions required to initiate swarming migration. Introduction of a rsbA mutation back into the wild type via allelic-exchange mutagenesis reconstructed the precocious swarming phenotype, which could be complemented in trans by a plasmid-borne copy of rsbA. Overexpression of RsbA in wild-type cells resulted in precocious swarming, suggesting that RsbA may have both positive and negative functions in regulating swarming migration. A possible model to describe the role of RsbA in swarming migration is discussed.
奇异变形杆菌的群游行为的特征是形成同心生长环，这些同心生长环是在菌落在表面迁移过程中，群体细胞分化、群游迁移和细胞分化的循环事件重复发生时形成的。这个循环产生了通常与奇异变形杆菌培养物相关的靶心菌落。目前尚不清楚细胞如何相互通信以协调这些完美同步的环。我们在此报告了一个基因位点的鉴定，该位点发生突变时会导致早熟群游表型。这些突变体在群游迁移的时间控制方面存在缺陷，比野生型细胞早约60分钟开始群游。与野生型不同，早熟群游突变体也是组成型群体细胞，并且在基本琼脂培养基上群游。发现这些缺陷定位于奇异变形杆菌基因组上一个5.4 kb的位点，该位点编码RsbA（群游行为调节因子）以及与RcsB和RcsC同源的奇异变形杆菌蛋白。RsbA与双组分调节蛋白家族的膜传感器组氨酸激酶同源，这表明RsbA可能作为启动群游迁移所需环境条件的传感器发挥作用。通过等位基因交换诱变将rsbA突变引入野生型中，重建了早熟群游表型，该表型可由携带rsbA的质粒在反式中互补。在野生型细胞中过表达RsbA导致早熟群游，这表明RsbA在调节群游迁移中可能具有正负两种功能。本文讨论了一个描述RsbA在群游迁移中作用的可能模型。
