Gimenez-Ibanez Selena, Hann Dagmar R, Ntoukakis Vardis, Petutschnig Elena, Lipka Volker, Rathjen John P
The Sainsbury Laboratory, Colney, Norwich NR4 7UH, UK.
Curr Biol. 2009 Mar 10;19(5):423-9. doi: 10.1016/j.cub.2009.01.054. Epub 2009 Feb 26.
Plant innate immunity relies on a set of pattern recognition receptors (PRRs) that respond to ligands known as pathogen-associated molecular patterns (PAMPs). To overcome such immunity, phytopathogenic bacteria deliver virulence molecules called effector proteins into the plant cell that collectively promote pathogenesis. The vast majority of PRRs controlling PAMP-triggered immunity (PTI) and the mechanisms used by specific effectors to suppress these pathways are mostly unknown. Here, we show that the Arabidopsis LysM receptor kinase CERK1, which is critical for chitin elicitor signaling and resistance to fungal pathogens, plays an essential role in restricting bacterial growth on plants. This is supported by the fact that CERK1 is a target of the bacterial type III effector protein AvrPtoB, which blocks all defense responses through this receptor. AvrPtoB ubiquitinates the CERK1 kinase domain in vitro and targets CERK1 for degradation in vivo. We show that CERK1 is a determinant of bacterial immunity, but its contribution is overcome by bacteria expressing AvrPtoB. Our results reveal a new pathway for plant immunity against bacteria and a role for AvrPtoB E3-ligase activity in suppressing PTI.
植物的先天免疫依赖于一组模式识别受体(PRR),这些受体对被称为病原体相关分子模式(PAMP)的配体作出反应。为了克服这种免疫,植物致病细菌将称为效应蛋白的毒力分子输送到植物细胞中,这些分子共同促进发病机制。绝大多数控制PAMP触发免疫(PTI)的PRR以及特定效应器抑制这些途径所使用的机制大多尚不清楚。在这里,我们表明拟南芥LysM受体激酶CERK1,其对几丁质激发子信号传导和对真菌病原体的抗性至关重要,在限制细菌在植物上的生长中起重要作用。这一观点得到了以下事实的支持:CERK1是细菌III型效应蛋白AvrPtoB的靶标,AvrPtoB通过该受体阻断所有防御反应。AvrPtoB在体外使CERK1激酶结构域泛素化,并在体内将CERK1作为降解目标。我们表明CERK1是细菌免疫的一个决定因素,但其作用被表达AvrPtoB的细菌所克服。我们的结果揭示了植物抗细菌免疫的一条新途径以及AvrPtoB E3连接酶活性在抑制PTI中的作用。