本项目的关注点是细胞自噬和三酰甘油代谢之间的关联。细胞自噬是一个基本的细胞生物学过程，主要负责高效清除胞内受损、冗余成分。三酰甘油是脂代谢的重要节点，是细胞贮存过剩碳源营养的主要形式。近年多项研究表明，自噬在三酰甘油相关的脂代谢过程中发挥重要作用。反之，对于三酰甘油代谢在自噬中的作用，目前研究尚不充分。我们在前期工作中发现：阻断三酰甘油的合成会显著抑制氮饥饿条件下的自噬，而阻断三酰甘油降解则基本不影响自噬。三酰甘油合成阻断情况下自噬的抑制源于自噬体形成的缺陷，具体缺陷步骤可能位于Atg1复合体或其下游。这些结果提示：三酰甘油合成涉及的某种中间代谢物可能具有抑制自噬的作用。在本项目中，我们将充分利用模式生物酵母中便捷的遗传学和细胞生物学工具，排查确定抑制自噬的关键代谢物，并在此基础上初步建立一条贯穿“关键代谢物-下游效用蛋白-关键自噬蛋白复合体”的自噬调控通路。

The focus of this project is the relationship between autophagy and triacylglycerol(TAG) metabolism. Autophagy is a fundamental cell biology process, which is essential in the efficient clearance of obsolete or damaged intracellular contents. TAG is a key node in lipid metabolism. It is a major storage form of excess carbon nutrient. The important roles of autophagy in TAG-related lipid metabolism have been demonstrated in several recent publications. Conversely, much less is known about the role of TAG metabolism in autophagy. Our preliminary data demonstrate that disruption of TAG synthesis results in severe inhibition of autophagy under nitrogen starvation conditions. In contrast, the influence of TAG consumption on autophagy is negligible. The observed inhibition of autophagy comes from reduced autophagosome biogenesis, possibly due to defects in the assembly of the Atg1 kinase complex or its downstream steps. These data suggest that the accumulation of certain metabolite(s) involved in TAG synthesis is inhibitory for autophagy. Taking advantage of the versatile genetic and cell biology tools in the budding yeast, here we seek to identify the critical autophagy-regulating compound, and to subsequently delineate a signaling pathway linking the critical metabolite(s), its downstream effector, and key Atg protein complex(es).