Structural Biology of CRISPR-Cas Surveillance Complexes
发布时间 :2019-10-10  阅读次数 :5388

报告人/Speaker: Prof. Dinshaw J. Patel

Member of National Academy of Sciences

Member of American Academy of Arts and Sciences

Memorial Sloan-Kettering Cancer Center

时间/Date: 20191025日(星期五),10:00-11:30

地点/Location: 闵行校区生物药学楼树华多功能厅报告厅



简介/Brief Bio:

Prof. Dinshaw Patel is an internationally renowned structural biologist, and has been a member of the American Academy of Sciences, and a member of the American Academy of Arts and Sciences. He is a Member and Abby Rockefeller Mauzé Chair in Experimental Therapeutics Structural Biology Program, Memorial Sloan-Kettering Cancer Center, an adjunct professor at Cornell University Weill Medical School, and a professor at the Southern University of Science and Technology. Dr. Patel has received numerous awards including Lifetime Achievement Award of the American Association of Indian Scientists in Cancer, Distinguished Alumnus Award. He has published over 520 research articles with over 50,000 citations.



The role of RNA in information transfer and catalysis highlights its dual functionalities. crRNA is a key component of CRISPR-Cas surveillance complexes.The lecture will initially address single-subunit Cas12 CRISPR-Cas systems involving ternary complexes with bound guide crRNA and target DNA. The emphasis will be on principles underlying PAM recognition and the conformation of the RuvC cleavage pocket.The lecture will next focus on multi-subunit CRISPR-Cas systems. For the type III-A Csm system, we shall address mechanisms of target RNA binding and cleavage, as well as target RNA-activated ssDNA cleavage in the HEPN pocket and cyclic oligoadenylate (cOA) formation from ATP in the Palm pocket. We will also highlight a timer mechanism for RNase Csm6 whereby successive nicks of bound cOA within the CARF domain regulate the trans-acting RNase activity of the adjacent HEPN domain.We have also highlight the impact of anti-CRISPR proteins in suppressing single- and multi-subunit CRISPR-Cas host defense pathways.