The Arabidopsis Leucine-Rich Repeat Receptor-Like Kinases BAK1/SERK3 and BKK1/SERK4 Are Required for Innate Immunity to Hemibiotrophic and Biotrophic Pathogens
The Arabidopsis Leucine-Rich Repeat Receptor-Like Kinases BAK1/SERK3 and BKK1/SERK4 Are Required for Innate Immunity to Hemibiotrophic and Biotrophic Pathogens
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DOI：
10.1105/tpc.111.084301
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发表时间：
2011-06-01
期刊：
影响因子：
11.6
通讯作者：
Zipfel, Cyril
中科院分区：
文献类型：
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作者：
Roux, Milena;Schwessinger, Benjamin;Zipfel, Cyril
表面定位模式识别受体（PRR）对病原体相关分子模式（PAMP）的识别构成了植物先天免疫的重要层。富含亮氨酸重复序列 (LRR) 受体激酶 EF-TU 受体 (EFR) 和 FLAGELLIN SENSING2 (FLS2) 是肽 PAMP elf18 和 flg22 的 PRR，它们分别源自细菌 EF-Tu 和鞭毛蛋白。使用免疫共沉淀和质谱分析，我们证明 EFR 和 FLS2 在植物中与属于体细胞胚胎发生受体样激酶 (SERK) 家族的几种 LRR 受体样激酶发生配体诱导的异聚化，包括油菜素类固醇不敏感 1 相关激酶 1/SERK3 (BAK1/SERK3) 和BAK1-LIKE1/SERK4 (BKK1/SERK4)。使用在油菜素类固醇和细胞死亡反应中不表现出多效性缺陷的新型 bak1 等位基因，我们确定 BAK1 和 BKK1 在遗传上合作以实现对 elf18 和 flg22 以及损伤相关分子模式 AtPep1 的完整信号传导能力。此外，我们证明 BAK1 和 BKK1 有助于对抗半生物营养细菌丁香假单胞菌和专性生物营养卵菌拟南芥操作菌 (Hyaloperonospora arabidopsidis) 的抗病性。我们的工作揭示了 PAMP 触发免疫 (PTI) 的建立依赖于配体诱导的 PRR 复合物中多个 SERK 的快速募集，并提供了对植物先天免疫这一重要层背后的早期 PTI 信号事件的深入了解。
Recognition of pathogen-associated molecular patterns (PAMPs) by surface-localized pattern recognition receptors (PRRs) constitutes an important layer of innate immunity in plants. The leucine-rich repeat (LRR) receptor kinases EF-TU RECEPTOR (EFR) and FLAGELLIN SENSING2 (FLS2) are the PRRs for the peptide PAMPs elf18 and flg22, which are derived from bacterial EF-Tu and flagellin, respectively. Using coimmunoprecipitation and mass spectrometry analyses, we demonstrated that EFR and FLS2 undergo ligand-induced heteromerization in planta with several LRR receptor-like kinases that belong to the SOMATIC-EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) family, including BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1/SERK3 (BAK1/SERK3) and BAK1-LIKE1/SERK4 (BKK1/SERK4). Using a novel bak1 allele that does not exhibit pleiotropic defects in brassinosteroid and cell death responses, we determined that BAK1 and BKK1 cooperate genetically to achieve full signaling capability in response to elf18 and flg22 and to the damage-associated molecular pattern AtPep1. Furthermore, we demonstrated that BAK1 and BKK1 contribute to disease resistance against the hemibiotrophic bacterium Pseudomonas syringae and the obligate biotrophic oomycete Hyaloperonospora arabidopsidis. Our work reveals that the establishment of PAMP-triggered immunity (PTI) relies on the rapid ligand-induced recruitment of multiple SERKs within PRR complexes and provides insight into the early PTI signaling events underlying this important layer of plant innate immunity.