An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis
An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis
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DOI：
10.1038/s41467-019-08783-0
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发表时间：
2019-02-15
影响因子：
16.6
通讯作者：
Parker, Jane E.
中科院分区：
文献类型：
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作者：
Bhandari, Deepak D.;Lapin, Dmitry;Parker, Jane E.
植物细胞内NLR受体识别病原体干扰以触发免疫，但NLR信号如何尚不清楚。增强的疾病易感性1（EDS 1）异二聚体被Toll-白细胞介素1受体结构域NLR（TNL）募集以转录动员抗性途径。通过询问拟南芥EDS 1 α-螺旋EP-结构域，我们确定了带正电荷的残基内衬一个腔，是必不可少的TNL免疫信号，超越异二聚体的形成。突变一个单一的，保守的表面精氨酸（R493）禁用TNL免疫卵菌病原体和细菌产生的毒力因子，冠菌素。表达弱活性EDS 1（R493 A）变体的植物具有延迟的转录重编程，对抗性和对抗细菌冠状病毒素对早期免疫基因的抑制具有严重后果。相同的EP结构域表面被非TNL受体RPS 2用于细菌免疫，表明EDS 1 EP结构域在由不同NLR受体类型赋予的抗性中发出信号。这些数据为NLR受体免疫中的早期下游信号传导提供了独特的结构见解。
Plant intracellular NLR receptors recognise pathogen interference to trigger immunity but how NLRs signal is not known. Enhanced disease susceptibility1 (EDS1) heterodimers are recruited by Toll-interleukin1-receptor domain NLRs (TNLs) to transcriptionally mobilise resistance pathways. By interrogating the Arabidopsis EDS1 alpha-helical EP-domain we identify positively charged residues lining a cavity that are essential for TNL immunity signalling, beyond heterodimer formation. Mutating a single, conserved surface arginine (R493) disables TNL immunity to an oomycete pathogen and to bacteria producing the virulence factor, coronatine. Plants expressing a weakly active EDS1(R493A) variant have delayed transcriptional reprogramming, with severe consequences for resistance and countering bacterial coronatine repression of early immunity genes. The same EP-domain surface is utilised by a non-TNL receptor RPS2 for bacterial immunity, indicating that the EDS1 EP-domain signals in resistance conferred by different NLR receptor types. These data provide a unique structural insight to early downstream signalling in NLR receptor immunity.