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• W2003108613 abstract "Subcellular localization is emerging as an important mechanism for mTORC1 regulation. We report that the tuberous sclerosis complex (TSC) signalling node, TSC1, TSC2 and Rheb, localizes to peroxisomes, where it regulates mTORC1 in response to reactive oxygen species (ROS). TSC1 and TSC2 were bound by peroxisomal biogenesis factors 19 and 5 (PEX19 and PEX5), respectively, and peroxisome-localized TSC functioned as a Rheb GTPase-activating protein (GAP) to suppress mTORC1 and induce autophagy. Naturally occurring pathogenic mutations in TSC2 decreased PEX5 binding, and abrogated peroxisome localization, Rheb GAP activity and suppression of mTORC1 by ROS. Cells lacking peroxisomes were deficient in mTORC1 repression by ROS, and peroxisome-localization-deficient TSC2 mutants caused polarity defects and formation of multiple axons in neurons. These data identify a role for the TSC in responding to ROS at the peroxisome, and identify the peroxisome as a signalling organelle involved in regulation of mTORC1. Reactive oxygen species inhibit mTORC1 signalling, but the subcellular localization of this event has been unclear. Walker and colleagues show that the tuberous sclerosis complex (TSC) is located at the peroxisome, where it functions as a Rheb GTPase-activator protein to suppress mTORC1 and induce autophagy. They also show that disease-associated mutations in TCS2 display impaired peroxisome localization and mTORC1 repression." @default.
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• W2003108613 date "2013-08-18" @default.
• W2003108613 modified "2023-10-16" @default.
• W2003108613 title "A tuberous sclerosis complex signalling node at the peroxisome regulates mTORC1 and autophagy in response to ROS" @default.
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• W2003108613 doi "https://doi.org/10.1038/ncb2822" @default.
• W2003108613 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3789865" @default.
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