bat365中文官网登录入口2013学年秋季学期系列学术讲座之一
题目：Clock Sugar Rush!
报告人：Yinghui Fu
Professor, Department of Neurology, School of Medicine, University of California, San Francisco
时间：2013年9月27日（周五），下午13:00-14:30 PM
地点：bat365中文官网登录入口一楼邓祐才报告厅
Sleep disruption has been shown to have significant impact on human health, quality of life, and life expectancy. In contrast to sleep quantity (where very limited is known), there is a wealth of information on the genetics of clock function across species. Sleep and circadian function are distinct processes that interact in living organisms. Although these two systems can operate independently, recent studies indicate a more intimate relationship.
Over the last decade, we have collected genetic material from individuals and families with circadian rhythm disturbances including familial advanced sleep phase (FASP) and familial delayed sleep phase (FDSP). To date, two genetic causes of FASPS have been reported. One is due to a mutation in PER2, a homologue of the first gene determined to be necessary for a proper circadian rhythm. The other is due to a mutation in a gene encoding a protein kinase called Casein Kinase I delta (CKIδ). By studying these two mutations, we have gained significant understanding deeper into the molecular mechanism of clock regulation.
In recent years, we have embarked on two separate circadian phospho-proteomic projects. Each of these investigations revealed to us new insight in both circadian regulation on biological pathways and the multi-layer modulation system of the molecular clock itself. We found that glucose levels through O-GlcNAcylation can modulate circadian clock providing evidence that nutrient intake (and its timing) and circadian clock have closely maintained cooperative relationship. Our data represents a further step toward a greater understanding of the complex mechanisms that control our bodily circadian functions in a highly coordinated manner.
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欢迎各位老师和同学积极参加！