Schmitt C K, Darnell S C, O'Brien A D
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, F. Edward Hèbert School of Medicine, Bethesda, MD 20814-4799, USA.
FEMS Microbiol Lett. 1996 Jan 15;135(2-3):281-5. doi: 10.1111/j.1574-6968.1996.tb08002.x.
FlgM inhibits the flagella-specific sigma factor FliA and is involved in the mouse-virulence of Salmonella typhimurium. In recent experiments, we observed that: (i) a flgM gene that could function to negatively regulate flagella synthesis was present in a variety of salmonellae; and (ii) the flgM gene derived from Salmonella species that are not normally virulent in mice could complement the S. typhimurium flgM mutant for virulence. Our results suggest that a functional flgM has been retained in most, and perhaps all, Salmonella species, regardless of the motility or virulence phenotype of the strain.
FlgM抑制鞭毛特异性σ因子FliA,并参与鼠伤寒沙门氏菌的小鼠毒力。在最近的实验中,我们观察到:(i) 能对鞭毛合成起负调控作用的flgM基因存在于多种沙门氏菌中;(ii) 源自通常对小鼠无毒力的沙门氏菌物种的flgM基因可补充鼠伤寒沙门氏菌flgM突变体的毒力。我们的结果表明,无论菌株的运动性或毒力表型如何,大多数甚至所有沙门氏菌物种中都保留了功能性flgM。