Structure of the lysosomal KICSTOR-GATOR1-SAMTOR nutrient-sensing supercomplex

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Authors: Christopher J. Lupton, Charles Bayly-Jones, Shuqi Dong, Terrance Lam, Wentong Luo, Gareth D. Jones, Chantel Mastos, Nicholas J. Frescher, San S. Lim, Alastair C. Keen, Luke E. Formosa, Hari Venugopal
+3 more Yong-Gang Chang, Michelle L. Halls, Andrew M. Ellisdon
Cited by: 6
References: 56

Abstract

The guanosine triphosphate (GTP)-bound state of the heterodimeric Rag GTPases functions as a molecular switch regulating mechanistic target of rapamycin complex 1 (mTORC1) activation at the lysosome downstream of amino acid fluctuations. Under low amino acid conditions, GTPase-activating protein (GAP) activity toward Rags 1 (GATOR1) promotes RagA GTP hydrolysis, preventing mTORC1 activation. KICSTOR recruits and regulates GATOR1 at the lysosome by undefined mechanisms. Here, we resolve the KICSTOR-GATOR1 structure, revealing a striking ∼60-nm crescent-shaped assembly. GATOR1 anchors to KICSTOR via an extensive interface, and mutations that disrupt this interaction impair mTORC1 regulation. The S-adenosylmethionine sensor SAMTOR binds KICSTOR in a manner incompatible with metabolite binding, providing structural insight into methionine sensing via SAMTOR-KICSTOR association. We discover that KICSTOR and GATOR1 form a dimeric supercomplex. This assembly restricts GATOR1 to an orientation that favors the low-affinity active GAP mode of Rag GTPase engagement while sterically restricting access to the high-affinity inhibitory mode, consistent with a model of an active lysosomal GATOR1 docking complex.

Fields of Study & Subjects

PI3K/AKT/mTOR signaling in cancer Cellular transport and secretion Microtubule and mitosis dynamics

Publication details

Journal / source
Cell
Publisher
Elsevier BV
Volume
189
Issue
4
Pages
1185–1200.e28
Publication date
8 January 2026
Language
EN