上睑下垂
炎症体
细胞生物学
生物
劈理(地质)
效应器
半胱氨酸蛋白酶
半胱氨酸蛋白酶1
生物化学
程序性细胞死亡
细胞凋亡
受体
断裂(地质)
古生物学
作者
Charles Lee Evavold,Iva Hafner‐Bratkovič,Pascal Devant,Jasmin M. D’Andrea,Elsy M. Ngwa,Elvira Boršić,John G. Doench,Martin W. LaFleur,Arlene H. Sharpe,Jay R. Thiagarajah,Jonathan C. Kagan
出处
期刊:Cell
[Cell Press]
日期:2021-07-21
卷期号:184 (17): 4495-4511.e19
被引量:417
标识
DOI:10.1016/j.cell.2021.06.028
摘要
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).
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