A TSC signaling node at the peroxisome regulates mTORC1 and autophagy in response to ROS

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A TSC signaling node at the peroxisome regulates mTORC1 and autophagy in response to ROS

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Title: A TSC signaling node at the peroxisome regulates mTORC1 and autophagy in response to ROS
Author: Zhang, Jiangwei; Kim, Jinhee; Alexander, Angela; Cai, Shengli; Tripathi, Durga Nand; Dere, Ruhee; Tee, Andrew R.; Tait-Mulder, Jacqueline; Di Nardo, Alessia; Han, Juliette M.; Kwiatkowski, Erica; Dunlop, Elaine A.; Dodd, Kayleigh M.; Folkerth, Rebecca D.; Faust, Phyllis L.; Kastan, Michael B.; Sahin, Mustafa; Walker, Cheryl Lyn

Note: Order does not necessarily reflect citation order of authors.

Citation: Zhang, J., J. Kim, A. Alexander, S. Cai, D. N. Tripathi, R. Dere, A. R. Tee, et al. 2013. “A TSC signaling node at the peroxisome regulates mTORC1 and autophagy in response to ROS.” Nature cell biology 15 (10): 1186-1196. doi:10.1038/ncb2822. http://dx.doi.org/10.1038/ncb2822.
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Abstract: Subcellular localization is emerging as an important mechanism for mTORC1 regulation. We report that the tuberous sclerosis complex (TSC) signaling 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 PEX19 and PEX5, respectively, and peroxisome-localized TSC functioned as a Rheb GAP to suppress mTORC1 and induce autophagy. Naturally occurring pathogenic mutations in TSC2 decreased PEX5 binding, 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 TSC in responding to ROS at the peroxisome, and identify the peroxisome as a signaling organelle involved in regulation of mTORC1.
Published Version: doi:10.1038/ncb2822
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3789865/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:12153037
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