Department of Biochemistry and Pharmacology and Bio21 Molecular Science and Biotechnology Institute and.
School of Physics, The University of Melbourne, Melbourne, Victoria 3010, Australia.
Mol Biol Cell. 2023 Apr 1;34(4):ar23. doi: 10.1091/mbc.E22-07-0302. Epub 2023 Feb 3.
The mechanistic target of rapamycin (mTOR) kinase regulates a major signaling pathway in eukaryotic cells. In addition to regulation of mTORC1 at lysosomes, mTORC1 is also localized at other locations. However, little is known about the recruitment and activation of mTORC1 at nonlysosomal sites. To identify regulators of mTORC1 recruitment to nonlysosomal compartments, novel interacting partners with the mTORC1 subunit, Raptor, were identified using immunoprecipitation and mass spectrometry. We show that one of the interacting partners, Arf5, is a novel regulator of mTORC1 signaling at plasma membrane ruffles. Arf5-GFP localizes with endogenous mTOR at PI3,4P2-enriched membrane ruffles together with the GTPase required for mTORC1 activation, Rheb. Knockdown of Arf5 reduced the recruitment of mTOR to membrane ruffles. The activation of mTORC1 at membrane ruffles was directly demonstrated using a plasma membrane-targeted mTORC1 biosensor, and Arf5 was shown to enhance the phosphorylation of the mTORC1 biosensor substrate. In addition, endogenous Arf5 was shown to be required for rapid activation of mTORC1-mediated S6 phosphorylation following nutrient starvation and refeeding. Our findings reveal a novel Arf5-dependent pathway for recruitment and activation of mTORC1 at plasma membrane ruffles, a process relevant for spatial and temporal regulation of mTORC1 by receptor and nutrient stimuli.
雷帕霉素靶蛋白(mTOR)激酶是真核细胞中主要信号通路的作用靶点。除了在溶酶体上对 mTORC1 进行调节外,mTORC1 还定位于其他位置。然而,对于 mTORC1 在非溶酶体部位的募集和激活知之甚少。为了鉴定 mTORC1 募集到非溶酶体区室的调节剂,我们使用免疫沉淀和质谱法鉴定了与 mTORC1 亚基 Raptor 相互作用的新的相互作用伙伴。我们发现,相互作用伙伴之一的 Arf5 是质膜皱襞中 mTORC1 信号的新型调节因子。Arf5-GFP 与内源性 mTOR 一起定位于富含 PI3,4P2 的质膜皱襞中,与激活 mTORC1 所需的 GTPase Rheb 一起定位。Arf5 的敲低减少了 mTOR 向质膜皱襞的募集。使用质膜靶向的 mTORC1 生物传感器直接证明了 mTORC1 在质膜皱襞上的激活,并且证明 Arf5 增强了 mTORC1 生物传感器底物的磷酸化。此外,内源性 Arf5 被证明是营养饥饿和再喂养后快速激活 mTORC1 介导的 S6 磷酸化所必需的。我们的研究结果揭示了一种新的 Arf5 依赖性途径,用于在质膜皱襞上募集和激活 mTORC1,这是受体和营养刺激对 mTORC1 进行时空调节的过程。