西湖名师论坛第二十六期 Westlake Master Forum Hongtao Yu：Mitotic checkpoint regulators in chromosome segregation
来源：wias 发布时间：2019-01-04 作者： 阅读数：341次
Time: 14 Jan 2019, 15:00-16:00
Venue: Lecture Hall, Building 5, Yunqi Campus
主持人: 西湖大学校长、结构生物学讲席教授 施一公
Host: Yigong Shi, Chair Professor, President of Westlake University
Prof. Hongtao Yu
Professor of Pharmacology at the University of Texas (UT) Southwestern Medical Center at Dallas, Investigator at the Howard Hughes Medical Institute (HHMI)
He received his B.S. in Chemistry from Peking University (Beijing, China) in 1990. He went to the United States to pursue his graduate studies, and received his Ph.D. in Chemistry from Harvard University (Cambridge, MA) in 1995. His thesis research with Dr. Stuart Schreiber focused on the structure determination of protein modules in signal transduction by nuclear magnetic resonance (NMR) spectroscopy. He then completed his postdoctoral training (1995-1999) with Dr. Marc Kirschner at Harvard Medical School (Boston, MA). During his postdoctoral training, Dr. Yu studied the composition, function, and regulation of the anaphase-promoting complex or cyclosome (APC/C), a multisubunit ubiquitin ligase critical for cell cycle progression. Dr. Yu began his independent research career in 1999 in the Department of Pharmacology at UT Southwestern Medical Center, and was promoted to Associate Professor with tenure in 2004 and to Professor in 2008. He was selected as an HHMI Investigator in 2008, and was elected a Fellow of the American Association for the Advancement of Science (AAAS) in 2012. Using a multidisciplinary approach, his lab has contributed significantly to our molecular understanding of chromosome segregation and genome maintenance.
Genome instability, including aneuploidy, causes human developmental diseases, cancer, and premature aging. The spindle checkpoint ensures accurate chromosome segregation during mitosis and guards against aneuploidy. In response to kinetochores not attached the mitotic spindle, the checkpoint proteins MAD2 and BUBR1 prevent premature anaphase onset. The MAD2 inhibitor p31comet promotes checkpoint inactivation and timely chromosome segregation. We have discovered a key cellular mechanism for sensing unattached kinetochores and have reconstituted checkpoint activation in the test tube with recombinant proteins. In addition, we have explored the physiological function of p31comet in the mouse. We show that the p31comet–MAD2–BUBR1 module regulates insulin signaling. Insulin regulates glucose and lipid metabolism and cell growth, and impacts many facets of animal physiology. Liver-specific ablation of p31comet in mice causes defects in insulin signaling and diabetes. Our findings link guardians of chromosome stability to nutrient metabolism and provide a clear example of evolutionary repurposing of a cell division module for metabolic regulation.
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