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Galectins control mTOR in response to endomembrane damage

ABSTRACT: 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.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Vojo Deretic

PROVIDER: MSV000081788 | MassIVE | Thu Dec 07 09:49:00 GMT 2017

SECONDARY ACCESSION(S): PXD008390

REPOSITORIES: MassIVE

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