报告题目：Antiphage defense by CARF-effector and protective deity systems
报告人：Dinshaw J. Patel 教授
主持人：任艾明 资深研究员
时 间：2026年8月4日（周二）下午3点
地 点：纳米楼457报告厅
报告人简介：
Dinshaw Patel received his B.S. in chemistry from the University of Mumbai and his Ph.D. in chemistry from New York University followed by postdoctoral work at NYU Medical School and AT&T Bell Laboratories. He next took a permanent appointment at Bell Laboratories as a Distinguished Member of Technical Staff for 17 years. He moved to Columbia University Medical Center as a Professor in 1984, and in 1992 took the Abby Rockefeller Mauze Chair at Memorial Sloan-Kettering to launch its Structural Biology program. His research has focused on the structural biology of riboswitches and ribozymes, RNA interference, readout of histone and DNA epigenetic marks, the cGAS-STING pathway, CRISPR-Cas surveillance complexes, SMC complexes, and most recently, bacterial antiphage defense pathways. He was elected to the National Academy of Sciences in 2009 and to the American Academy of Arts and Sciences in 2014. He has been awarded the Tan Jiazhen International Life Sciences Collaboration Award in 2019, the Shizhang Bei International Award in 2023, and was made an Honorary Professor of Tsinghua University in 2024.
报告摘要：
The arms race between bacteria and viruses has given rise to the dynamic pan-genome composed of a combination of bacterial sensor-effector surveillance complexes. Following viral infection, a viral trigger activates the sensor protein, that in turn activates effector proteins, thereby promoting antiviral defense through either targeted nuclease activity, depletion of cellular metabolites or disruption of host cell membrane functions. Notably, antiviral defense capitalizes on an abortive infection mechanism, whereby infected cells die prior to completion of the phage replication cycle, insuring survival of the colony. Given that these systems have developed multiple, sophisticated avenues of active defense, in the process collectively constituting an “immune system”, it is critical to deduce a mechanistic understanding of these diverse defense pathways, thereby opening new opportunities for biotechnological and biomedical applications. The first half of the lecture will focus on type III CRISPR-generated cyclic oligoadenylates (cOAs) that target CARF domains to activate linked effector domains.The second half of the lecture will capitalize on the richness of newly identified prokaryotic antiviral defense systems, opening opportunities for characterizing the diversity of mechanisms of bacterial antiviral immunity and its evolutionary adaptation by metazoans.
