The protein kinase mTOR (mechanistic target of rapamycin) pathways play crucial roles in regulating cell growth, survival, and metabolism in response to changes in cellular energy and nutrient status. Despite significant efforts, our understanding of mTOR pathways still has many gaps that need to be filled. To address the knowledge gaps, our research will focus on three directions. Firstly, we will investigate the mechanisms by which mTOR controls the initiation and termination of autophagy. Although our knowledge in this area has significantly improved, we still do not clearly understand how post-translational modifications, interactions, and translocations of autophagy regulators are coordinated to drive autophagy initiation. Furthermore, while mTOR regulates autophagy termination, the underlying mechanisms remain elusive. Secondly, we will investigate how cells decide between autophagy, mitophagy, and apoptosis during energy crisis caused by mitochondrial dysfunction. Our recent study has challenged the long-held notion that autophagy is responsible for supplying energy to energy-deprived cells for survival. Contrary to the prevailing concept, we found that energy-deprived cells restrain autophagy and mitophagy via activating AMPK, the major energy sensor kinase in mammalian cells. Our research has revealed previously unrecognized roles of ULK1, the central kinase that regulates autophagy downstream of mTOR, in the crosstalk between autophagy, mitochondria, and apoptosis. This finding highlights the critical importance of maintaining functional mitochondria for autophagy. Investigating the coordination mechanism underlying the crosstalk between autophagy, mitophagy, and apoptosis during energy stress is crucial for a comprehensive understanding of cellular energetics for cell survival. Thirdly, we will investigate the functions of mTOR in different cellular compartments. The majority of previous studies have focused on lysosomal mTOR, with limited explanation of how lysosomal mTOR controls protein synthesis and autophagy initiation that primarily occur in the endoplasmic reticulum. While non-lysosomal functions of mTOR have recently emerged, their roles in different cellular compartments remain largely unexplored. Through our single-molecule analysis, we have learned that the majority of mTOR exists in non-lysosomal compartments and that some forms of non-lysosomal mTOR are responsive to amino acids, providing unprecedented insights into mTOR distribution and regulation in various cellular locations. Addressing this critical knowledge gap is essential for elucidating previously unrecognized functions of mTOR. Through these three directions of research, our study aims to advance fundamental knowledge on mTOR functions in coordinating nutrient, growth, and energy status with autophagy, mitophagy, and cell survival. Additionally, the outcomes of this study are expected to provide crucial insights into the cellular pathways for energy sensing and ...