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Ragulator-Rag-mTORC1 通路对 GSDMD 寡聚化和细胞焦亡的调控作用。

Control of gasdermin D oligomerization and pyroptosis by the Ragulator-Rag-mTORC1 pathway.

机构信息

Division of Gastroenterology, Boston Children's Hospital and Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.

Division of Gastroenterology, Boston Children's Hospital and Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA; Department of Synthetic Biology and Immunology, National Institute of Chemistry, Hajdrihova 19, 1000 Ljubljana, Slovenia; EN-FIST Centre of Excellence, Trg Osvobodilne fronte 13, 1000 Ljubljana, Slovenia.

出版信息

Cell. 2021 Aug 19;184(17):4495-4511.e19. doi: 10.1016/j.cell.2021.06.028. Epub 2021 Jul 21.

Abstract

The process of pyroptosis is mediated by inflammasomes and a downstream effector known as gasdermin D (GSDMD). Upon cleavage by inflammasome-associated caspases, the N-terminal domain of GSDMD forms membrane pores that promote cytolysis. Numerous proteins promote GSDMD cleavage, but none are known to be required for pore formation after GSDMD cleavage. Herein, we report a forward genetic screen that identified the Ragulator-Rag complex as being necessary for GSDMD pore formation and pyroptosis in macrophages. Mechanistic analysis revealed that Ragulator-Rag is not required for GSDMD cleavage upon inflammasome activation but rather promotes GSDMD oligomerization in the plasma membrane. Defects in GSDMD oligomerization and pore formation can be rescued by mitochondrial poisons that stimulate reactive oxygen species (ROS) production, and ROS modulation impacts the ability of inflammasome pathways to promote pore formation downstream of GSDMD cleavage. These findings reveal an unexpected link between key regulators of immunity (inflammasome-GSDMD) and metabolism (Ragulator-Rag).

摘要

细胞焦亡过程由炎性小体和一种称为 Gasdermin D (GSDMD) 的下游效应蛋白所介导。在炎性小体相关半胱天冬酶的切割作用下,GSDMD 的 N 端结构域形成促进细胞裂解的膜孔。许多蛋白促进 GSDMD 切割,但在 GSDMD 切割后,没有已知的蛋白是形成孔所必需的。在此,我们报告了一项正向遗传学筛选,该筛选确定 Ragulator-Rag 复合物是巨噬细胞中 GSDMD 孔形成和细胞焦亡所必需的。机制分析表明,Ragulator-Rag 在炎性小体激活时不需要 GSDMD 切割,但在质膜中促进 GSDMD 寡聚化。GSDMD 寡聚化和孔形成缺陷可被刺激活性氧 (ROS) 产生的线粒体毒物挽救,并且 ROS 调节会影响炎性小体途径在 GSDMD 切割下游促进孔形成的能力。这些发现揭示了免疫(炎性小体-GSDMD)和代谢(Ragulator-Rag)关键调节因子之间的意外联系。

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本文引用的文献

1
Genome-wide CRISPR screens reveal multitiered mechanisms through which mTORC1 senses mitochondrial dysfunction.
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2
NINJ1 mediates plasma membrane rupture during lytic cell death.
Nature. 2021 Mar;591(7848):131-136. doi: 10.1038/s41586-021-03218-7. Epub 2021 Jan 20.
3
Structural insights into TSC complex assembly and GAP activity on Rheb.
Nat Commun. 2021 Jan 12;12(1):339. doi: 10.1038/s41467-020-20522-4.
4
Succination inactivates gasdermin D and blocks pyroptosis.
Science. 2020 Sep 25;369(6511):1633-1637. doi: 10.1126/science.abb9818. Epub 2020 Aug 20.
5
The Immunomodulatory Metabolite Itaconate Modifies NLRP3 and Inhibits Inflammasome Activation.
Cell Metab. 2020 Sep 1;32(3):468-478.e7. doi: 10.1016/j.cmet.2020.07.016. Epub 2020 Aug 12.
6
FDA-approved disulfiram inhibits pyroptosis by blocking gasdermin D pore formation.
Nat Immunol. 2020 Jul;21(7):736-745. doi: 10.1038/s41590-020-0669-6. Epub 2020 May 4.
7
Structural Mechanism for GSDMD Targeting by Autoprocessed Caspases in Pyroptosis.
Cell. 2020 Mar 5;180(5):941-955.e20. doi: 10.1016/j.cell.2020.02.002. Epub 2020 Feb 27.
8
mTOR at the nexus of nutrition, growth, ageing and disease.
Nat Rev Mol Cell Biol. 2020 Apr;21(4):183-203. doi: 10.1038/s41580-019-0199-y. Epub 2020 Jan 14.
9
Cryo-EM Structure of the Human FLCN-FNIP2-Rag-Ragulator Complex.
Cell. 2019 Nov 27;179(6):1319-1329.e8. doi: 10.1016/j.cell.2019.10.036. Epub 2019 Nov 6.
10
Inflammasome signaling and regulation of interleukin-1 family cytokines.
J Exp Med. 2020 Jan 6;217(1). doi: 10.1084/jem.20190314.

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