MassIVE MSV000081788

Partial Public PXD008390

Galectins control mTOR in response to endomembrane damage

Description

The Ser/Thr protein kinase mTOR controls metabolic pathways, including the catabolic process of autophagy. Autophagy plays additional, catabolism-independent roles in homeostasis of cytoplasmic endomembranes and whole organelles. How signals from endomembrane damage are transmitted to mTOR to orchestrate autophagic responses is not known. Here we show that mTOR is inhibited by lysosomal damage. Lysosomal damage, recognized by galectins, leads to association of Gal8 with mTOR apparatus on the lysosome. Gal8 inhibits mTOR activity through its Ragulator-Rag signaling machinery. Thus, a novel galectin-based signal-transduction apparatus, termed here GALTOR, controls mTOR in response to lysosomal damage. [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: mTOR ; Galectins ; endomembrane

Contact

Principal Investigators:
(in alphabetical order)
Vojo Deretic, University of New Mexico Health Sciences Center, USA
Submitting User: brettsp1
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