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mTORC2: The other mTOR in autophagy regulation
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mTORC2: The other mTOR in autophagy regulation
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Journal Article
mTORC2: The other mTOR in autophagy regulation
2021
Overview
The mechanistic target of rapamycin (mTOR) has gathered significant attention as a ubiquitously expressed multimeric kinase with key implications for cell growth, proliferation, and survival. This kinase forms the central core of two distinct complexes, mTORC1 and mTORC2, which share the ability of integrating environmental, nutritional, and hormonal cues but which regulate separate molecular pathways that result in different cellular responses. Particularly, mTORC1 has been described as a major negative regulator of endosomal biogenesis and autophagy, a catabolic process that degrades intracellular components and organelles within the lysosomes and is thought to play a key role in human health and disease. In contrast, the role of mTORC2 in the regulation of autophagy has been considerably less studied despite mounting evidence this complex may regulate autophagy in a different and perhaps complementary manner to that of mTORC1. Genetic ablation of unique subunits is currently being utilized to study the differential effects of the two mTOR complexes. RICTOR is the best‐described subunit specific to mTORC2 and as such has become a useful tool for investigating the specific actions of this complex. The development of complex‐specific inhibitors for mTORC2 is also an area of intense interest. Studies to date have demonstrated that mTORC1/2 complexes each signal to a variety of exclusive downstream molecules with distinct biological roles. Pinpointing the particular effects of these downstream effectors is crucial toward the development of novel therapies aimed at accurately modulating autophagy in the context of human aging and disease. mTORC2 is a negative regulator of macroautophagy and chaperone‐mediated autophagy via its ability to signal to various downstream effectors shown to modulate autophagy in mammals including AKT, PKC, SGK‐1, and FOXO transcription factors. In this review, we highlight the importance of identifying novel mechanisms that target mTORC2 specifically but also of dissecting the role of the downstream effectors through substrate‐specific interactions.
