西亚试剂：Receptor-like Cytoplasmic Kinases Integrate Signaling from

Receptor-like Cytoplasmic Kinases Integrate Signaling from Multiple Plant Immune Receptors and Are Targeted by a Pseudomonas syringae Effector
Jie Zhang1, 4, Wei Li1, 4, Tingting Xiang1, 2, Zixu Liu1, Kristin Laluk3, Xiaojun Ding1, Yan Zou1, Minghui Gao1, Xiaojuan Zhang1, She Chen1, Tesfaye Mengiste3, Yuelin Zhang1 and Jian-Min Zhou1, ,

1 National Institute of Biological Sciences, Beijing 102206, China
2 State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100094, China
3 Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN 47907, USA

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.

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