Schmitt C K, Darnell S C, Tesh V L, Stocker B A, O'Brien A D
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799.
J Bacteriol. 1994 Jan;176(2):368-77. doi: 10.1128/jb.176.2.368-377.1994.
Salmonella typhimurium ST39 exhibits reduced virulence in mice and decreased survival in mouse macrophages compared with the parent strain SL3201. Strain ST39 is nonmotile, carries an indeterminate deletion in and near the flgB operon, and is defective in the mviS (mouse virulence Salmonella) locus. In flagellum-defective strains, the flgM gene product of S. typhimurium negatively regulates flagellar genes by inhibiting the activity of FliA, the flagellin-specific sigma factor. In this study, flgM of wild-type S. typhimurium LT2 was found to complement the mviS defect in ST39 for virulence in mice and for enhanced survival in macrophages. Transduction of flgM::Tn10dCm into the parent strain SL3201 resulted in attenuation of mouse virulence and decreased survival in macrophages. However, a flgM-fliA double mutant was fully virulent in mice and survived in macrophages at wild-type levels. Thus, the absolute level of FliA activity appears to affect the virulence of S. typhimurium SL3201 in mice. DNA hybridization studies showed that flgM-related sequences were present in species other than Salmonella typhimurium and that sequences related to that of fliA were common among members of the family Enterobacteriaceae. Our results demonstrate that flgM and fliA, two genes previously shown to regulate flagellar operons, are also involved in the regulation of expression of virulence of S. typhimurium and that this system may not be unique to the genus Salmonella.
与亲本菌株SL3201相比，鼠伤寒沙门氏菌ST39在小鼠中的毒力降低，在小鼠巨噬细胞中的存活率降低。ST39菌株无运动能力，在flgB操纵子及其附近存在不确定的缺失，并且在mviS（小鼠毒力沙门氏菌）位点存在缺陷。在鞭毛缺陷型菌株中，鼠伤寒沙门氏菌的flgM基因产物通过抑制鞭毛蛋白特异性σ因子FliA的活性来负调节鞭毛基因。在本研究中，发现野生型鼠伤寒沙门氏菌LT2的flgM可弥补ST39中mviS缺陷对小鼠的毒力以及在巨噬细胞中提高的存活率。将flgM::Tn10dCm转导至亲本菌株SL3201导致小鼠毒力减弱和在巨噬细胞中的存活率降低。然而，flgM - fliA双突变体在小鼠中具有完全毒力，并且在巨噬细胞中的存活率与野生型水平相当。因此，FliA活性的绝对水平似乎影响鼠伤寒沙门氏菌SL3201在小鼠中的毒力。DNA杂交研究表明，flgM相关序列存在于鼠伤寒沙门氏菌以外的物种中，并且与fliA相关的序列在肠杆菌科成员中很常见。我们的结果表明，flgM和fliA这两个先前显示可调节鞭毛操纵子的基因也参与了鼠伤寒沙门氏菌毒力表达的调节，并且该系统可能并非沙门氏菌属所特有。
