부산대학교 도서관

The mechanistic target of rapamycin complex 1 (mTORC1) signaling hub integrates multiple environmental cues to modulate cell growth and metabolism. Over the past decade considerable knowledge has been gained on the mechanisms modulating mTORC1 lysosomal recruitment and activation. However, whether and how mTORC1 is able to elicit selective responses to diverse signals has remained elusive until recently. We discuss emerging evidence for a 'non-canonical' mTORC1 signaling pathway that controls the function of microphthalmia/transcription factor E (MiT-TFE) transcription factors, key regulators of cell metabolism. This signaling pathway is mediated by a specific mechanism of substrate recruitment, and responds to stimuli that appear to converge on the lysosomal surface. We discuss the relevance of this pathway in physiological and disease conditions. Mechanistic target of rapamycin complex 1 (mTORC1) mediates selective metabolic responses to diverse environmental cues by differential activation of a canonical and a non-canonical signaling pathway. Non-canonical mTORC1 signaling responds to stimuli that converge on the lysosomal surface. Rag GTPases mediate a novel mTORC1 substrate-recruitment mechanism. Deregulation of non-canonical mTORC1 signaling underlies the pathogenesis of different types of inherited diseases and cancer. [ABSTRACT FROM AUTHOR]