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4月20日学术讲座 罗招庆教授

来源:研究生教学  浏览量:  更新时间:2017-04-20 10:34:06

报告题目:Bacterial secretion systems, their effectors and targets for anti-infection strategies

报 告 人:罗招庆教授 (吉林大学第一医院,普渡大学生物科学系)

邀 请 人:陈 实 教授

报告时间:2017年4月20日下午4点

时间地点:武汉大学文理学部测试中心一楼会议室


 

报告人简介:

,1991年获北京农业大学学士学位,2001年伊利依大学厄巴那-香分校博士学位,2004年起任普渡大学,2015年升正教授。2017年加盟吉林大学第一医院。主要从事病原生物学,细菌-寄主相互作用机理和宿主免疫的机理研究,阐明病原细菌侵染的生化和细胞生物学基础。近年通过解析多个新的酶功能,揭示了新的感染机理和寄主细胞的信号传递机制。最近发现的独立于E1/E2 的泛素修饰催化机理引起了细胞生物学领域的极大关注,Nature, Molecular Cell, Current Biology, Nature Review Microbiology,Cell Host & Microbe 和 Science Signaling 等杂志刊发了评论和介绍,并被 Science Signaling 杂志选为2016年“细胞信号传导”领域十大突破之一。 担任NIH、中国自然科学基金、以色列自然科学基金、加拿大生部基金等的委。PLoS Pathogens 委 (Associate Editor)。

 

报告摘要:

Specialized secretion systems are essential pathogenic elements in many important pathogens. The study of effectors injected into host cells by these systems has provided novel insights into not only the mechanism of infection but also novel signaling mechanisms in eukaryotes. In this talk, I will discuss some of our recent progress in determining the function of Legionella pneumophila effectors effectors and their modulation of host defense mechanisms with an emphasis on our recent discovery of a single protein-catalyzed, ATP-independent ubiquitination mechanism and its regulation. In contrast to canonical ubiquitination involved in E1, E2 and E3 enzymes that function sequentially to covalently attach ubiquitin to the substrate, we found that members of SidE effector family activate ubiquitin via ADP-ribosylation at Arg42 of the ubiquitin molecule. Following up studies from other research groups demonstrate that ADP-ribosylated ubiquitin is cleaved by a phosphodiesterase activity within the same protein and the phosphoribosylated ubiquitin is linked to serine residues of target proteins. We also found that this unique ubiquitination is reversed by another bacterial protein to impose temporal regulation on the activity of the ligases. Finally, I will briefly discuss our work in the development of anti-virulence strategies by targeting type III secretion systems of Salmonella enterica Typhimurium.