Zheng Rikuan, Wu Shimei, Ma Ning, Sun Chaomin
Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.
Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao, China.
Front Microbiol. 2018 Apr 5;9:682. doi: 10.3389/fmicb.2018.00682. eCollection 2018.
Mercury-mediated toxicity remains one of the greatest barriers against microbial survival, even though bacterial resistance to mercury compounds can occur. However, the genetic and physiological adaptations of bacteria to mercury stress still remains unclear. Here, we show that the marine bacterium 273 is resistant to 50 μM Hg and removes up to 94% Hg from culture. Using gene homologous recombination and complementation, we show that genes encoding Hg-transport proteins MerT, MerP, the mercuric reductase MerA and the regulatory protein MerD are essential for bacterial mercuric resistance when challenged with Hg. Further, mercury stress inhibits flagellar development, motility, chemotaxis and biofilm formation of 273, which are verified by transcriptomic and physiological analyses. Surprisingly, we discover that MerF, a previously reported Hg-transporter, determines flagellar development, motility and biofilm formation in 273 by genetic and physiological analyses. Our results strongly indicate that MerF plays an integral role in 273 to develop physiological responses to mercury stress. Notably, MerF homologs are also prevalent in different human pathogens. Using this unique target may provide novel strategies to control these pathogenic bacteria, given the role of MerF in flagella and biofilm formation. In summary, our data provide an original report on MerF in bacterial physiological development and suggest that the in marine bacteria has evolved through progressive, sequential recruitment of novel functions over time.
汞介导的毒性仍然是微生物生存面临的最大障碍之一,尽管细菌可能会对汞化合物产生抗性。然而,细菌对汞胁迫的遗传和生理适应性仍不清楚。在此,我们表明海洋细菌273对50μM汞具有抗性,并能从培养物中去除高达94%的汞。通过基因同源重组和互补实验,我们发现当受到汞挑战时,编码汞转运蛋白MerT、MerP、汞还原酶MerA和调节蛋白MerD的基因对于细菌的汞抗性至关重要。此外,汞胁迫会抑制273的鞭毛发育、运动性、趋化性和生物膜形成,这已通过转录组学和生理学分析得到证实。令人惊讶的是,通过遗传和生理学分析,我们发现先前报道的汞转运蛋白MerF决定了273的鞭毛发育、运动性和生物膜形成。我们的结果有力地表明,MerF在273对汞胁迫产生生理反应中起着不可或缺的作用。值得注意的是,MerF同源物在不同的人类病原体中也很普遍。鉴于MerF在鞭毛和生物膜形成中的作用,利用这个独特的靶点可能为控制这些病原菌提供新策略。总之,我们的数据提供了关于MerF在细菌生理发育方面的原始报告,并表明海洋细菌中的 随着时间的推移通过逐步、连续地获得新功能而进化。