Avruch Joseph, Long Xiaomeng, Ortiz-Vega Sara, Rapley Joseph, Papageorgiou Angela, Dai Ning
Department of Molecular Biology and Diabetes Research Unit, Medical Service, Massachusetts General Hospital, and Department of Medicine, Harvard Medical School, Simches Research Center, Boston, MA 02114, USA.
Am J Physiol Endocrinol Metab. 2009 Apr;296(4):E592-602. doi: 10.1152/ajpendo.90645.2008. Epub 2008 Sep 2.
TOR complex 1 (TORC1), an oligomer of the mTOR (mammalian target of rapamycin) protein kinase, its substrate binding subunit raptor, and the polypeptide Lst8/GbetaL, controls cell growth in all eukaryotes in response to nutrient availability and in metazoans to insulin and growth factors, energy status, and stress conditions. This review focuses on the biochemical mechanisms that regulate mTORC1 kinase activity, with special emphasis on mTORC1 regulation by amino acids. The dominant positive regulator of mTORC1 is the GTP-charged form of the ras-like GTPase Rheb. Insulin, growth factors, and a variety of cellular stressors regulate mTORC1 by controlling Rheb GTP charging through modulating the activity of the tuberous sclerosis complex, the Rheb GTPase activating protein. In contrast, amino acids, especially leucine, regulate mTORC1 by controlling the ability of Rheb-GTP to activate mTORC1. Rheb binds directly to mTOR, an interaction that appears to be essential for mTORC1 activation. In addition, Rheb-GTP stimulates phospholipase D1 to generate phosphatidic acid, a positive effector of mTORC1 activation, and binds to the mTOR inhibitor FKBP38, to displace it from mTOR. The contribution of Rheb's regulation of PL-D1 and FKBP38 to mTORC1 activation, relative to Rheb's direct binding to mTOR, remains to be fully defined. The rag GTPases, functioning as obligatory heterodimers, are also required for amino acid regulation of mTORC1. As with amino acid deficiency, however, the inhibitory effect of rag depletion on mTORC1 can be overcome by Rheb overexpression, whereas Rheb depletion obviates rag's ability to activate mTORC1. The rag heterodimer interacts directly with mTORC1 and may direct mTORC1 to the Rheb-containing vesicular compartment in response to amino acid sufficiency, enabling Rheb-GTP activation of mTORC1. The type III phosphatidylinositol kinase also participates in amino acid-dependent mTORC1 activation, although the site of action of its product, 3'OH-phosphatidylinositol, in this process is unclear.
雷帕霉素靶蛋白复合体1(TORC1)是由雷帕霉素哺乳动物靶蛋白(mTOR)蛋白激酶、其底物结合亚基 Raptor以及多肽Lst8/GβL组成的寡聚体,它能响应营养物质的可利用性,在所有真核生物中控制细胞生长;在多细胞动物中,它还能响应胰岛素、生长因子、能量状态和应激条件来控制细胞生长。本综述聚焦于调节mTORC1激酶活性的生化机制,特别强调氨基酸对mTORC1的调节作用。mTORC1的主要正向调节因子是类Ras GTP酶Rheb的GTP结合形式。胰岛素、生长因子和多种细胞应激源通过调节结节性硬化复合体(Rheb GTP酶激活蛋白)的活性来控制Rheb的GTP结合,从而调节mTORC1。相反,氨基酸,尤其是亮氨酸,通过控制Rheb-GTP激活mTORC1的能力来调节mTORC1。Rheb直接与mTOR结合,这种相互作用似乎对mTORC1的激活至关重要。此外,Rheb-GTP刺激磷脂酶D1生成磷脂酸,磷脂酸是mTORC1激活的正向效应物,并且Rheb-GTP与mTOR抑制剂FKBP38结合,将其从mTOR上置换下来。相对于Rheb直接与mTOR结合,Rheb对PL-D1和FKBP38的调节对mTORC1激活的贡献仍有待充分明确。Rag GTP酶作为必需的异二聚体发挥作用,也是mTORC1氨基酸调节所必需的。然而,与氨基酸缺乏的情况一样,Rag缺失对mTORC1的抑制作用可通过Rheb过表达来克服,而Rheb缺失则消除了Rag激活mTORC1的能力。Rag异二聚体直接与mTORC1相互作用,并且在氨基酸充足时,可能将mTORC1引导至含有Rheb的囊泡区室,从而使Rheb-GTP激活mTORC1。III型磷脂酰肌醇激酶也参与了氨基酸依赖性的mTORC1激活,尽管其产物3'-OH-磷脂酰肌醇在此过程中的作用位点尚不清楚。