Sonnleitner Elisabeth, Hagens Steven, Rosenau Frank, Wilhelm Susanne, Habel André, Jäger Karl-Erich, Bläsi Udo
Max F. Perutz Laboratories, Department of Microbiology and Genetics, University Departments at the Vienna Biocenter, University of Vienna, Dr Bohrgasse 9, 1030 Vienna, Austria.
Microb Pathog. 2003 Nov;35(5):217-28. doi: 10.1016/s0882-4010(03)00149-9.
The Sm-like protein Hfq has been implicated in the regulation of sigmaS-dependent and sigmaS-independent genes in E. coli and in the regulation of virulence factors in both, Yersinia enterocolitica and Brucella abortus. Here, we have studied the effect of Hfq on virulence and stress response of Pseudomonas aeruginosa (PAO1). We have constructed a PAO1hfq- mutant and a PAO1hfq-rpoS- double mutant to permit distinction between direct and indirect effects of Hfq. When compared to the wild-type and the rpoS- strains, the hfq knock out strain showed a reduced growth rate and was unable to utilize glucose as a sole carbon source. Elastase activity was 80% reduced in the hfq- mutant when compared to the wild-type or the rpoS- strain, whereas alginate production seemed to be solely affected by sigmaS. The production of catalase and pyocyanin was shown to be affected in an additive manner by both, Hfq and sigmaS. Moreover, twitching and swarming mediated by typeIV pili was shown to be impaired in the hfq- mutant. When compared to PAO1 wild-type and the rpoS- mutant, the hfq- mutant decreased virulence in Galleria mellonella by a factor of 1 x 10(4) and 5 x 10(3), respectively. Likewise, when compared to wild-type, the PAO1hfq- mutant was significantly attenuated in virulence when administered intraperitoneally in mice. These results strongly suggest that Hfq is a global regulator of PAO1 virulence and stress response which is not exclusively due to its role in stimulating the synthesis of sigmaS.
类Sm蛋白Hfq参与了大肠杆菌中依赖σS和不依赖σS的基因调控,以及小肠结肠炎耶尔森氏菌和流产布鲁氏菌中致病因子的调控。在此,我们研究了Hfq对铜绿假单胞菌(PAO1)毒力和应激反应的影响。我们构建了PAO1hfq-突变体和PAO1hfq-rpoS-双突变体,以区分Hfq的直接和间接作用。与野生型和rpoS-菌株相比,hfq基因敲除菌株的生长速率降低,且无法利用葡萄糖作为唯一碳源。与野生型或rpoS-菌株相比,hfq-突变体的弹性蛋白酶活性降低了80%,而藻酸盐的产生似乎仅受σS的影响。过氧化氢酶和绿脓菌素的产生显示受到Hfq和σS的叠加影响。此外,hfq-突变体中由IV型菌毛介导的颤动和群游运动受损。与PAO1野生型和rpoS-突变体相比,hfq-突变体使大蜡螟的毒力分别降低了1×10⁴倍和5×10³倍。同样,与野生型相比,PAO1hfq-突变体经腹腔注射给小鼠时毒力显著减弱。这些结果强烈表明,Hfq是PAO1毒力和应激反应的全局调节因子,这并非完全归因于其在刺激σS合成中的作用。