报告主题：Physiology and Pathology of Glutamate Receptor Protein Stability for Excitatory Synapse
报告人：盛能印 研究员（中国科学院昆明动物研究所）
邀请人：朱金伟 研究员
时间：5月30日（周二）13:30—16:00
地点：徐汇校区小白楼201A会议室
报告人简介：
盛能印，研究员，博士生导师。2003年毕业于南开大学生命科学学院生物科学专业，获理学学士学位；2011年毕业于中国科学院上海生物化学与细胞生物学研究所，发育生物学专业，获理学博士学位；2011-2017年在美国加州大学旧金山分校细胞与分子药理系从事博士后研究；2017年8月至今，中国科学院昆明动物研究所，遗传资源与进化国家重点实验室，大脑进化发育与生理功能学科组课题组长；入选中国科学院百人计划、云南省“云岭英才计划”云岭高层次人才；主持国家自然科学基金委面上项目、云南省“杰出青年”和重点项目等课题。
报告摘要:
The accurate expression of postsynaptic AMPA receptors (AMPARs) is critical for information processing in the brain, and ubiquitination is a key regulator for this biological process. However, the roles and mechanisms of AMPARs protein stability regulators are poorly understood. Here, we find that the ubiquitination and protein stability of AMPARs are regulated by neurological disorder-related molecules RNF220 and ZC4H2. Therefore, RNF220 or ZC4H2 knockout specifically increases AMPAR protein levels, thereby enhancing basal synaptic activity while impairing synaptic plasticity. Moreover, depending on its protein stability activity, RNF220 or ZC4H2 represses AMPAR-mediated excitatory synaptic responses and their neuronal surface expression. Furthermore, learning and memory are altered in forebrain RNF220 or ZC4H2-deficient mice. Besides, through the above synaptopathological mechanisms, the neurological disorder mutations of RNF220 or ZC4H2 are involved in synaptic activity and neural behavior regulation. Together, we identify RNF220 and ZC4H2 as protein stability modulator for AMPARs in neurons and establish their substantial roles in excitatory synaptic transmission and brain function.
