Laboratory of Chemical Biology and Microbial Pathogenesis , The Rockefeller University , New York , New York 10065 , United States.
ACS Chem Biol. 2019 Mar 15;14(3):405-414. doi: 10.1021/acschembio.8b01038. Epub 2019 Feb 20.
The peptidoglycan fragments γ-d-glutamyl- meso-diaminopimelic acid (iE-DAP) and muramyl-dipeptide (MDP) are microbial-specific metabolites that activate intracellular pattern recognition receptors and stimulate immune signaling pathways. While extensive structure-activity studies have demonstrated that these bacterial cell wall metabolites trigger NOD1- and NOD2-dependent signaling, their direct binding to these innate immune receptors or other proteins in mammalian cells has not been established. To characterize these fundamental microbial metabolite-host interactions, we synthesized a series of peptidoglycan metabolite photoaffinity reporters and evaluated their cross-linking to NOD1 and NOD2 in mammalian cells. We show that active iE-DAP and MDP photoaffinity reporters selectively cross-linked NOD1 and NOD2, respectively, and not their inactive mutants. We also discovered MDP reporter cross-linking to Arf GTPases, which interacted most prominently with GTP-bound Arf6 and coimmunoprecipitated with NOD2 upon MDP stimulation. Notably, MDP binding to NOD2 and Arf6 was abrogated with loss-of-function NOD2 mutants associated with Crohn's disease. Our studies demonstrate peptidoglycan metabolite photoaffinity reporters can capture their cognate immune receptors in cells and reveal unpredicted ligand-induced interactions with other cellular cofactors. These photoaffinity reporters should afford useful tools to discover and characterize other peptidoglycan metabolite-interacting proteins.
肽聚糖片段γ-D-谷氨酰基-内消旋二氨基庚二酸(iE-DAP)和 muramyl-二肽(MDP)是微生物特异性代谢物,可激活细胞内模式识别受体并刺激免疫信号通路。虽然广泛的结构-活性研究表明这些细菌细胞壁代谢物触发 NOD1 和 NOD2 依赖性信号传导,但它们与这些先天免疫受体或哺乳动物细胞中的其他蛋白质的直接结合尚未确定。为了表征这些基本的微生物代谢物-宿主相互作用,我们合成了一系列肽聚糖代谢物光亲和报告物,并评估了它们在哺乳动物细胞中与 NOD1 和 NOD2 的交联。我们表明,活性 iE-DAP 和 MDP 光亲和报告物分别选择性地交联 NOD1 和 NOD2,而不是它们的非活性突变体。我们还发现 MDP 报告物与 Arf GTPases 交联,这些 GTPases 与 GTP 结合的 Arf6 相互作用最显著,并在 MDP 刺激时与 NOD2 共免疫沉淀。值得注意的是,MDP 与 NOD2 和 Arf6 的结合被与克罗恩病相关的功能丧失 NOD2 突变体所阻断。我们的研究表明,肽聚糖代谢物光亲和报告物可以在细胞中捕获其同源免疫受体,并揭示与其他细胞辅助因子的意外配体诱导相互作用。这些光亲和报告物应该为发现和表征其他肽聚糖代谢物相互作用蛋白提供有用的工具。