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HmsC响应氧化还原环境控制生物膜形成。

HmsC Controls Biofilm Formation in Response to Redox Environment.

作者信息

Ren Gai-Xian, Guo Xiao-Peng, Sun Yi-Cheng

机构信息

MOH Key Laboratory of Systems Biology of Pathogens, Institute of Pathogen Biology, Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing, China.

出版信息

Front Cell Infect Microbiol. 2017 Aug 8;7:355. doi: 10.3389/fcimb.2017.00355. eCollection 2017.

Abstract

biofilm formation, controlled by intracellular levels of the second messenger molecule cyclic diguanylate (c-di-GMP), is important for blockage-dependent plague transmission from fleas to mammals. HmsCDE is a tripartite signaling system that modulates intracellular c-di-GMP levels to regulate biofilm formation in . Previously, we found that biofilm formation is stimulated in reducing environments in an -dependent manner. However, the mechanism by which HmsCDE senses the redox state remains elusive. Using a mutant and the addition of Cu to simulate reducing and oxidizing periplasmic environments, we found that HmsC protein levels are decreased and the HmsC-HmsD protein-protein interaction is weakened in a reducing environment. In addition, we revealed that intraprotein disulphide bonds are critical for HmsC since breakage lowers protein stability and diminishes the interaction with HmsD. Our results suggest that HmsC might play a major role in sensing the environmental changes.

摘要

由第二信使分子环二鸟苷酸(c-di-GMP)的细胞内水平控制的生物膜形成,对于跳蚤向哺乳动物的堵塞依赖性鼠疫传播很重要。HmsCDE是一个三方信号系统,可调节细胞内c-di-GMP水平以调节生物膜形成。以前,我们发现生物膜形成在还原环境中以依赖于的方式受到刺激。然而,HmsCDE感知氧化还原状态的机制仍然难以捉摸。使用突变体并添加铜来模拟还原和氧化的周质环境,我们发现在还原环境中HmsC蛋白水平降低,并且HmsC-HmsD蛋白-蛋白相互作用减弱。此外,我们发现蛋白质内二硫键对HmsC至关重要,因为断裂会降低蛋白质稳定性并减少与HmsD的相互作用。我们的结果表明,HmsC可能在感知环境变化中起主要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74bc/5550408/07eb64904170/fcimb-07-00355-g0001.jpg

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