植物抗病性涉及通过细胞表面模式识别受体检测微生物分子模式和通过细胞内NLR免疫受体检测病原体效应子。NLR分类为传感器NLR,参与效应子检测,或传感器NLR信令所需的助手NLR。含有TIR域的传感器NLR(TNL)需要辅助NLRNRG1和ADR1来获得电阻,防御的辅助NLR激活需要脂肪酶结构域蛋白EDS1,SAG101和PAD4。以前,我们发现NRG1以TNL激活依赖的方式与EDS1和SAG101结合[X.Sun等人。,纳特。Commun.12,3335(2021)]。我们在此报告在TNL启动的免疫期间,辅助NLRNRG1如何与其自身以及与EDS1和SAG101相关联。完全免疫需要细胞表面和细胞内免疫受体启动的信号传导的共激活和相互增强[B.P.M.Ngou,H.-K.安恩,P.丁,J.D.G.琼斯,Nature592,110-115(2021),M、袁等人。,自然592,105-109(2021)]。我们发现,虽然激活TNL足以促进NRG1-EDS1-SAG101相互作用,寡聚NRG1-EDS1-SAG101抗性体的形成需要细胞表面受体启动防御的额外共激活。这些数据表明,体内NRG1-EDS1-SAG101抗性体的形成是连接细胞内和细胞表面受体信号传导途径的机制的一部分。
Plant disease resistance involves both detection of microbial molecular patterns by cell-surface pattern recognition receptors and detection of pathogen effectors by intracellular NLR immune receptors. NLRs are classified as sensor NLRs, involved in effector detection, or helper NLRs required for sensor NLR signaling. TIR-domain-containing sensor NLRs (TNLs) require helper NLRs NRG1 and ADR1 for resistance, and helper NLR activation of defense requires the lipase-domain proteins EDS1, SAG101, and PAD4. Previously, we found that NRG1 associates with EDS1 and SAG101 in a TNL activation-dependent manner [X. Sun et al., Nat. Commun. 12, 3335 (2021)]. We report here how the helper NLR NRG1 associates with itself and with EDS1 and SAG101 during TNL-initiated immunity. Full immunity requires coactivation and mutual potentiation of cell-surface and intracellular immune receptor-initiated signaling [B. P. M. Ngou, H.-K. Ahn, P. Ding, J. D. G. Jones, Nature 592, 110-115 (2021), M. Yuan et al., Nature 592, 105-109 (2021)]. We find that while activation of TNLs is sufficient to promote NRG1-EDS1-SAG101 interaction, the formation of an oligomeric NRG1-EDS1-SAG101 resistosome requires the additional coactivation of cell-surface receptor-initiated defense. These data suggest that NRG1-EDS1-SAG101 resistosome formation in vivo is part of the mechanism that links intracellular and cell-surface receptor signaling pathways.