学术报告:Differential thiol-based switches jump-start Vibrio choleraepathogenesis

2015年12月03日 12:43  点击:[]

报告题目:Differential thiol-based switches jump-start Vibrio choleraepathogenesis
报告人: 朱军 教授
美国宾夕法尼亚大学佩雷尔曼医学院
报告时间:2015年3月11日(周三)下午2:00
报告地点:生物楼113室
报告人简介:朱军 (Jay Zhu),现任美国宾夕法尼亚大学佩雷尔曼医学院微生物学副教授,兼任克莱姆森大学、南京农业大学和上海交通大学教授,我校海天学者,长期从事病原微生物学研究,在霍乱弧菌的致病机理以及病原与宿主关系的研究上取得了卓越的成就,并在PNAS、Journal of Bacteriology、Journal of Biological Chemistry、Infection and Immunity等国际知名刊物上发表学术论文50余篇,担任Journal of Bacteriology、Frontiers in Microbiology、International Journal of Molecular Sciences等杂志的编委,以及Nature、PNAS、PLoS Pathogens等杂志的审稿人,同时还是中国国家自然科学基金海外评审专家及美国国家自然科学基金评审专家。
报告摘要:Bacterial pathogens have evolved sophisticated signal transduction systems to coordinately control the expression of virulence determinants. For example, the human pathogen Vibrio cholerae is able to respond to host environmental signals by activating transcriptional regulatory cascades. The host signals that stimulate V. cholerae virulence gene expression, however, are still poorly understood. Previous proteomic studies indicated that the ambient oxygen concentration plays a role in V. cholerae virulence gene expression. In this study, we found that under oxygen-limiting conditions, an environment similar to the intestines, V. choleraevirulence genes are highly expressed. We show that anaerobiosis enhances dimerization and activity of AphB, a transcriptional activator that is required for the expression of the key virulence regulator TcpP, which leads to the activation of virulence factor production. We further show that one of the three cysteine residues in AphB, C(235), is critical for oxygen responsiveness, as the AphB(C235S) mutant can activate virulence genes under aerobic conditions in vivo and can bind to tcpP promoters in the absence of reducing agents in vitro. Mass spectrometry analysis suggests that under aerobic conditions, AphB is modified at the C(235) residue. This modification is reversible between oxygen-rich aquatic environments and oxygen-limited human hosts, suggesting that V. cholerae may use a thiol-based switch mechanism to sense intestinal signals and activate virulence.



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