第十二期水木清华生命科学讲座系列
林圣彩教授
厦门大学特聘教授、“973”首席科学家,现任厦门大学生命科学学院院长。
林教授长期致力于细胞代谢稳态维持及其调控细胞生长的分子机制。先前发现了由GSK3激酶、乙酰转移酶TIP60、ULK1激酶组成的一条介导细胞在缺乏生长因子时诱导细胞自噬的信号转导通路。新近又发现了细胞在缺乏能量时所积累的AMP能自主地诱导一个基于Axin的蛋白质复合体的形成来激活能量感受激酶AMPK,在能量平衡的机制方面做出了重大发现。基于上述介导细胞自噬和能量平衡的分子机制的发现,继续开展细胞维持代谢稳态的生物学研究,包括自噬通路与细胞整体代谢调控的交叉的机制,在分子、细胞器、个体多水平上研究细胞代谢稳态调控与细胞生长的关系。在Science, Nature, Cell Metabolism, Oncogene, EMBO J等杂志上发表多篇高水平的SCI论文,被引用5000余次。“揭示营养匮乏引发细胞自噬的分子机制”获得2012年度“中国科学十大进展”。
题目: 代谢平衡控制的机制
Abstract:
Cells possess remarkable proteins that can sense the availability of nutrients and energy levels. Autophagy represents a key catabolic process that can recycle cellular components to sustain energy levels for survival under nutrient-poor conditions or growth factor deprivation. We previously delineated a pathway, in which glycogen synthase kinase 3 (GSK3) in cells deprived of growth factors, phosphorylates and activates the acetyltransferase TIP60, which in turn stimulates the protein kinase ULK1 to elicit autophagy. AMPK (AMP-activated protein kinase) plays a central role in maintaining cellular energy homeostasis. When cellular energy levels are low (increased AMP/ATP ratio), AMPK is activated to enhance catabolic activities with concurrent inhibition of anabolic processes such as fatty acid synthesis. In this seminar, I will present our recent discovery of a 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. This work has provided mechanistic insights into how AMP initiates activation of AMPK by LKB1.
Date: 3:00-4:00pm, Oct. 09 (Wednesday)
Venue: B323, Medical School Building