The Leucine-Rich Repeat Receptor Kinase BIR2 Is a Negative Regulator of BAK1 in Plant Immunity
The Leucine-Rich Repeat Receptor Kinase BIR2 Is a Negative Regulator of BAK1 in Plant Immunity
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DOI：
10.1016/j.cub.2013.11.047
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发表时间：
2014-01-20
期刊：
影响因子：
9.2
通讯作者：
Kemmerling, Birgit
中科院分区：
文献类型：
--
作者：
Halter, Thierry;Imkampe, Julia;Kemmerling, Birgit
背景：跨膜富含亮氨酸重复序列（LRR）受体是植物和动物中常用的先天免疫受体，但也可以感知内源信号来调节发育。 BAK1 是一种植物 LRR 受体样激酶 (RLK)，它与多个配体结合的 LRR-RLK 相互作用，以积极调节其功能。 BAK1 通过分别与油菜素类固醇受体 BRI1、免疫受体（例如 FLS2 和 EFR）以及小受体激酶 BIR1 相互作用，参与油菜素类固醇依赖性生长和发育、先天免疫和细胞死亡控制。结果：通过 LC/ESI-MS/MS 鉴定体内 BAK1 复合体伴侣，发现了两种新的 BAK1 相互作用 RLK：BIR2 和 BIR3。磷酸化研究表明，BIR2 被 BAK1 单向磷酸化，并且 BAK1 和 BIR2 之间的相互作用是激酶活性依赖性的。 bir2突变体的功能分析显示对BAK1调节过程的不同影响，例如对病原体相关分子模式（PAMP）的高反应性、增强的细胞死亡和对细菌病原体的抵抗力，但对油菜素类固醇调节的生长没有影响。 BIR2 与 BAK1 组成型相互作用，从而防止与配体结合的 LRR-RLK FLS2 相互作用。 PAMP 感知导致 BIR2 从 BAK1 复合物中释放，并使 BAK1 招募到 FLS2 复合物中。结论：我们的结果为先天免疫受体的新调节机制提供了证据，其中 BIR2 通过在没有配体的情况下限制 BAK1 受体复合物的形成，充当 PAMP 触发免疫的负调节因子。
Background: Transmembrane leucine-rich repeat (LRR) receptors are commonly used innate immune receptors in plants and animals but can also sense endogenous signals to regulate development. BAK1 is a plant LRR-receptor-like kinase (RLK) that interacts with several ligand-binding LRR-RLKs to positively regulate their functions. BAK1 is involved in brassinosteroid-dependent growth and development, innate immunity, and cell-death control by interacting with the brassinosteroid receptor BRI1, immune receptors, such as FLS2 and EFR, and the small receptor kinase BIR1, respectively. Results: Identification of in vivo BAK1 complex partners by LC/ESI-MS/MS uncovered two novel BAK1-interacting RLKs, BIR2 and BIR3. Phosphorylation studies revealed that BIR2 is unidirectionally phosphorylated by BAK1 and that the interaction between BAK1 and BIR2 is kinase-activity dependent. Functional analyses of bir2 mutants show differential impact on BAK1-regulated processes, such as hyperresponsiveness to pathogen-associated molecular patterns (PAMP), enhanced cell death, and resistance to bacterial pathogens, but have no effect on brassinosteroid-regulated growth. BIR2 interacts constitutively with BAK1, thereby preventing interaction with the ligand-binding LRR-RLK FLS2. PAMP perception leads to BIR2 release from the BAK1 complex and enables the recruitment of BAK1 into the FLS2 complex. Conclusions: Our results provide evidence for a new regulatory mechanism for innate immune receptors with BIR2 acting as a negative regulator of PAMP-triggered immunity by limiting BAK1-receptor complex formation in the absence of ligands.