报告人：林圣彩，厦门大学天美娱乐教授♌️、“长江学者”特聘教授
主持人：翁杰敏 教授
时 间✉️： 2015年11月16日下午14:00-15:30 （周一下午）
地 点🤶🏿：闵行校区天美娱乐534报告厅
报告人简介🧑🦯：林圣彩教授🏊♀️，厦门大学天美娱乐教授🚵🏿♂️、“长江学者”特聘教授。1984年获厦门大学生物学系学士学位; 1985年作为CUSBEA 项目留学生选送到美国攻读博士, 1991年获得美国美国西南医学中心（Southwestern Medical Center at Dallas）生物化学专业博士学位; 1991-1995年在美国加州大学圣地亚哥分校的霍华德休斯医学研究所从事博士后工作🧑🚀；1995-2001年新加坡分子与细胞生物学研究所任高级研究员（Senior Scientist）💷；2001-2006为香港科技大学助理教授👨👨👦👦、副教授（获终身职位）；2006年7月起全职回到厦门大学。2003年起任厦门大学天美娱乐院长。林圣彩教授近年致力于研究机体内控制细胞能量平衡的分子调控机制。在近年内🔘，“揭示营养匮乏引发细胞自噬的分子机制”方面的研究结果发表在2012年4月《Science》杂志上☣️，并入选科技部评选的2012年度“中国科学十大进展”🤙🏽；于2013🚃、2014连续在《Cell Metabolism》发表了揭示AMPK激活机制的文章, 揭示了AMP作为细胞低能量信号如何激活AMPK的分子机制，找到了细胞如何进行合成代谢与分解代谢的一个切换“开关”📼。现已在国际主流刊物发表论文80多篇，已被他人引用6000余次。曾获国家杰出青年科学基金𓀁、国家自然科学基金委“创新研究群体等资助， “973”计划项目首席科学家、入选“国家百千万工程人才” 。
报告内容简介：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. We also uncovered that AMPK is a residential protein of late endosome/lysosome. Under glucose starvation, the v-ATPase-Ragulator complex is accessible to AXIN/LKB1 for AMPK activation. Concurrently, mTORC dissociates from endosome. We have thus revealed a switch between catabolism and anabolism.
Most recently, we have uncovered other functions of ULK1/2 kinases than initiation of autophagy. We found that ULK1 functions to regulate glycolytic pathways by direct phosphorylation of multiple glycolytic enzymes. The functional outcome of the modulation of the enzymatic activities by ULK1 will be presented at the talk.
Publications:
1. Lin SY et al., GSK3-TIP60-ULK1 signaling pathway links growth factor deprivation to autophagy. Science 336, 477, 2012
2. Zhang YL et al., AMP as a low energy charge signal autonomously initiates assembly of AXIN-AMPK-LKB1 complex for AMPK activation. Cell Metabolism 18, 546–555, 2013
3. Zhang CS et al., The Lysosomal v-ATPase-Ragulator Complex is a Common Activator for AMPK and mTORC1, acting as a Switch between Catabolism and Anabolism. Cell Metabolism 20, 526-540, 2014
4. Zhang CS et al., RHOBTB3 promotes HIF1alpha proteasomal degradation through facilitating hydroxylation and suppresses the Warburg effect, Cell Res., 2015
5. Li TY et al., ULK1/2 in reprogramming of glucose fluxes, manuscript under review
