National Institute of Biological Sciences, Beijing 102206, China.
National Institute of Biological Sciences, Beijing 102206, China; State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100094, China.
Cell Host Microbe. 2010 Apr 22;7(4):290-301. doi: 10.1016/j.chom.2010.03.007.
Cell-surface-localized plant immune receptors, such as FLS2, detect pathogen-associated molecular patterns (PAMPs) and initiate PAMP-triggered immunity (PTI) through poorly understood signal-transduction pathways. The pathogenic Pseudomonas syringae effector AvrPphB, a cysteine protease, cleaves the Arabidopsis receptor-like cytoplasmic kinase PBS1 to trigger cytoplasmic immune receptor RPS5-specified effector-triggered immunity (ETI). Analyzing the function of AvrPphB in plants lacking RPS5, we find that AvrPphB can inhibit PTI by cleaving additional PBS1-like (PBL) kinases, including BIK1, PBL1, and PBL2. In unstimulated plants, BIK1 and PBL1 interact with FLS2 and are rapidly phosphorylated upon FLS2 activation by its ligand flg22. Genetic and molecular analyses indicate that BIK1, and possibly PBL1, PBL2, and PBS1, integrate immune signaling from multiple immune receptors. Whereas AvrPphB-mediated degradation of one of these kinases, PBS1, is monitored by RPS5 to initiate ETI, this pathogenic effector targets other PBL kinases for PTI inhibition.
细胞表面定位的植物免疫受体，如 FLS2，通过尚未完全理解的信号转导途径来检测病原体相关分子模式（PAMPs）并启动 PAMP 触发的免疫（PTI）。病原菌丁香假单胞菌效应物 AvrPphB 是一种半胱氨酸蛋白酶，可切割拟南芥受体样细胞质激酶 PBS1，引发细胞质免疫受体 RPS5 特异性效应物触发的免疫（ETI）。在缺乏 RPS5 的植物中分析 AvrPphB 的功能，我们发现 AvrPphB 可以通过切割包括 BIK1、PBL1 和 PBL2 在内的其他 PBS1 样（PBL）激酶来抑制 PTI。在未受刺激的植物中，BIK1 和 PBL1 与 FLS2 相互作用，并在 FLS2 被其配体 flg22 激活时迅速被磷酸化。遗传和分子分析表明，BIK1，可能还有 PBL1、PBL2 和 PBS1，整合了来自多种免疫受体的免疫信号。虽然 AvrPphB 介导的这些激酶之一 PBS1 的降解被 RPS5 监测以启动 ETI，但这种致病性效应物针对其他 PBL 激酶以抑制 PTI。
