A phospho-switch constrains BTL2-mediated phytocytokine signaling in plant immunity
A phospho-switch constrains BTL2-mediated phytocytokine signaling in plant immunity
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DOI：
10.1016/j.cell.2023.04.027
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发表时间：
2023-05
期刊：
影响因子：
64.5
通讯作者：
Xiao Yu;Yingpeng Xie;Dexian Luo;Hai Liu;M. V. D. Oliveira;Peipei Qi;Sung-Il Kim;F. A. Ortiz-Morea;Jun Liu;Yafei Chen;Sixue Chen;Bárbara Rodrigues;Bo Li;Shaowu Xue;Ping He;Libo Shan
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文献类型：
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作者：
Xiao Yu;Yingpeng Xie;Dexian Luo;Hai Liu;M. V. D. Oliveira;Peipei Qi;Sung-Il Kim;F. A. Ortiz-Morea;Jun Liu;Yafei Chen;Sixue Chen;Bárbara Rodrigues;Bo Li;Shaowu Xue;Ping He;Libo Shan
激活和限制免疫激活对维持细胞稳态至关重要。消耗多种模式识别受体（PRRs）的共受体BAK1和SERK4，会消除模式触发的免疫，但会触发细胞内nod样受体（NLR）介导的自身免疫，其机制尚不清楚。通过在拟南芥中部署基于rnai的遗传筛选，我们鉴定了BAK1 - to - life 2 (BTL2)，这是一种未知的受体激酶，可检测BAK1/SERK4的完整性。当BAK1/SERK4受到干扰时，BTL2通过激活Ca2+通道CNGC20以激酶依赖的方式诱导自身免疫。为了弥补BAK1缺失，BTL2与多种植物细胞因子受体复合物，导致由辅助NLR ADR1家族免疫受体介导的强效植物细胞因子反应，表明植物细胞因子信号是连接PRR和NLR介导的免疫的分子链接。值得注意的是，BAK1通过特异性磷酸化抑制BTL2的激活以维持细胞完整性。因此，BTL2作为监测变阻器，感知BAK1/SERK4免疫共受体的扰动，促进nlr介导的植物细胞因子信号传导，以确保植物免疫。
Enabling and constraining immune activation is of fundamental importance in maintaining cellular homeostasis. Depleting BAK1 and SERK4, the co-receptors of multiple pattern recognition receptors (PRRs), abolishes pattern-triggered immunity but triggers intracellular NOD-like receptor (NLR)-mediated autoimmunity with an elusive mechanism. By deploying RNAi-based genetic screens inArabidopsis, we identified BAK-TO-LIFE 2 (BTL2), an uncharacterized receptor kinase, sensing BAK1/SERK4 integrity. BTL2 induces autoimmunity through activating Ca2+channel CNGC20 in a kinase-dependent manner when BAK1/SERK4 are perturbed. To compensate for BAK1 deficiency, BTL2 complexes with multiple phytocytokine receptors, leading to potent phytocytokine responses mediated by helper NLR ADR1 family immune receptors, suggesting phytocytokine signaling as a molecular link connecting PRR- and NLR-mediated immunity. Remarkably, BAK1 constrains BTL2 activation via specific phosphorylation to maintain cellular integrity. Thus, BTL2 serves as a surveillance rheostat sensing the perturbation of BAK1/SERK4 immune co-receptors in promoting NLR-mediated phytocytokine signaling to ensure plant immunity.