IMM & CLS Research Seminar

Title：Mechanisms for sensing nutritional stresses and reprogramming of metabolic pathways

Speaker：林圣彩 教授

厦门大学生命科学学院院长

Time：2015年4月17日（星期五）下午2:00-3:00

Place：北京大学英杰交流中心306会议室

Host：北京大学分子医学研究所 刘颖 (Tel. 6276-6523)

Abstract：Metabolic homeostasis is maintained by various cellular sensors, including the master kinases AMPK (AMP-activated protein kinase) and mTORC1. In response to low energy status, AMPK is activated to enhance catabolic activities with concurrent inhibition of anabolic processes such as fatty acid synthesis. In contrast, mTORC1 is activated when nutrients and growth factors are abundant. Previously, we discovered the mechanism by which AMP, as a low energy-charge signal, can autonomously initiate the assembly of an activating complex for AMPK in response to starvation. AMP binding causes a higher affinity of AMPK for the scaffold protein AXIN that also binds to LKB1, thereby promoting phosphorylation and activation of AMPK. More recently, we found most surprisingly that the late endosomal/lysosomal protein complex v-ATPase-Ragulator, essential for activation of mTORC1, is also required for AMPK activation. Under glucose starvation, the v-ATPase-Ragulator complex is accessible to AXIN/LKB1 for AMPK activation and concomitantly dissociates mTORC1. We have thus revealed that the v-ATPase-Ragulator complex is also an initiating sensor for energy stress, thereby providing a switch between catabolism and anabolism. I will also present our most recent work on the function of ULK1/2 beyond autophagy.

欢迎各位老师同学积极参加！