从基因水平研究电活性希瓦氏菌Shewanella oneidensis MR-1的微生物腐蚀机制

微生物腐蚀在世界范围内造成严重的经济损失。传统理论认为微生物活动改变局部电化学环境导致腐蚀。近来研究发现很多电活性微生物通过细胞外电子传递从金属主动获得电子导致微生物腐蚀，即电子传递微生物腐蚀。电子传递微生物腐蚀理论的提出突破了传统理论的认知，但目前仍缺少基因层面的系统研究。申请者前期研究发现电活性希瓦氏菌MR-1通过细胞外电子传递显著加速316L不锈钢的腐蚀。本项目拟以此为基础，引入合成生物学、分子生物学、转录组学、生物信息学的技术手段从基因水平揭示电子载体介导的间接电子传递、Mtr电子传递通路介导的直接电子传递参与微生物腐蚀的分子作用机制，以及两种电子传递方式之间的协同作用机制，并深入分析电子传递微生物腐蚀的生理意义与实现方式以及本研究构建的电子传递机制在电活性微生物腐蚀中的普适性。相关研究将提供电子传递微生物腐蚀的系统分析与全新认识，并为电子传递微生物腐蚀的靶向防治提供理论指导。

Microbiologically influenced corrosion (MIC) causes tremendous economic losses throughout the world. Traditional theories of MIC holds that the electrochemical changes in local environments resulted from microbial activity lead to metal corrosion. However, current studies have found many electroactive microorganisms can actively acquire electrons from metal surfaces through extracellular electron transfer (EET), which leads to MIC and is called EET-MIC. The EET-MIC theory breaks through the basic concepts of traditional theory, but there is still a lack of systematic research at the gene level. Our previous study found that the electroactive Shewanella oneidensis MR-1 significantly accelerated corrosion of 316L stainless steel through extracellular electron transfer. Based on this, this project will introduce the technology of synthetic biology, molecular biology, transcriptomics, and bioinformatics to reveal the molecular mechanism of the indirect electron transfer mediated by electron shuttles, and the direct electron transfer mediated by Metal-reducing conduit (Mtr conduit) at the gene level. Meanwhile, the cooperative mechanisms between these two electron transfer modes during the MIC process will be elucidated. The physiological significance and implementation processes of EET-MIC will be analyzed in-depth. Moreover, the general applicability of the EET-MIC mechanism illustrated in this study will be verified through performing comparative genomics analysis with other electroactive microorganisms that are corrosive. The results of this project will provide a systematic analysis and creative cognition to the mechanism of EET-MIC, and provide a theoretical guidance for the targeted prevention and control of EET-MIC.