美国德州农工大学Libo Shan等研究人员合作发现,一个磷酸化开关限制BTL2在植物免疫中介导的植物细胞因子信号传递。相关论文于2023年5月15日在线发表在《细胞》杂志上。
研究人员表示,启用和限制免疫激活在维持细胞平衡方面具有根本的重要性。消耗BAK1和SERK4,即多种模式识别受体(PRR)的共同受体,可以取消模式触发的免疫,但会引发细胞内NOD样受体(NLR)介导的自身免疫,其机制难以捉摸。
通过在拟南芥中进行基于RNAi的遗传筛选,研究人员发现了BAK-TO-LIFE 2(BTL2),一个未被鉴定的受体激酶,感知BAK1/SERK4的完整性。当BAK1/SERK4受到干扰时,BTL2通过以激酶依赖的方式激活Ca2+通道CNGC20,诱发自身免疫。为了弥补BAK1的不足,BTL2与多种植物细胞因子受体复合,导致由辅助性NLR ADR1家族免疫受体介导的强有力的植物细胞因子反应,表明植物细胞因子信号是连接PRR-和NLR介导的免疫的分子环节。值得注意的是,BAK1通过特定的磷酸化制约BTL2的激活,以维持细胞的完整性。因此,BTL2在促进NLR介导的植物细胞因子信号传递来确保植物免疫力方面充当了感知BAK1/SERK4免疫共受体扰动的监视变调器。
附:英文原文
Title: A phospho-switch constrains BTL2-mediated phytocytokine signaling in plant immunity
Author: Xiao Yu, Yingpeng Xie, Dexian Luo, Hai Liu, Marcos V.V. de Oliveira, Peipei Qi, Sung-Il Kim, Fausto Andres Ortiz-Morea, Jun Liu, Yafei Chen, Sixue Chen, Bárbara Rodrigues, Bo Li, Shaowu Xue, Ping He, Libo Shan
Issue&Volume: 2023-05-15
Abstract: Enabling and constraining immune activation is of fundamental importance in maintainingcellular homeostasis. Depleting BAK1 and SERK4, the co-receptors of multiple patternrecognition receptors (PRRs), abolishes pattern-triggered immunity but triggers intracellularNOD-like receptor (NLR)-mediated autoimmunity with an elusive mechanism. By deployingRNAi-based genetic screens in Arabidopsis, we identified BAK-TO-LIFE 2 (BTL2), an uncharacterized receptor kinase, sensingBAK1/SERK4 integrity. BTL2 induces autoimmunity through activating Ca2+ channel CNGC20 in a kinase-dependent manner when BAK1/SERK4 are perturbed. To compensatefor BAK1 deficiency, BTL2 complexes with multiple phytocytokine receptors, leadingto potent phytocytokine responses mediated by helper NLR ADR1 family immune receptors,suggesting phytocytokine signaling as a molecular link connecting PRR- and NLR-mediatedimmunity. Remarkably, BAK1 constrains BTL2 activation via specific phosphorylationto maintain cellular integrity. Thus, BTL2 serves as a surveillance rheostat sensingthe perturbation of BAK1/SERK4 immune co-receptors in promoting NLR-mediated phytocytokinesignaling to ensure plant immunity.
DOI: 10.1016/j.cell.2023.04.027
Source: https://www.cell.com/cell/fulltext/S0092-8674(23)00423-3
本期文章:《细胞》:Online/在线发表