Nuclear accumulation of the Arabidopsis immune receptor RPS4 is necessary for triggering EDS1-dependent defense

Nuclear accumulation of the Arabidopsis immune receptor RPS4 is necessary for triggering EDS1-dependent defense
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DOI:
10.1016/j.cub.2007.10.042
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发表时间:
2007-12-04
期刊:
影响因子:
9.2
通讯作者:
Parker, Jane E.
Parker, Jane E.
中科院分区:
生物学1区
文献类型:
--
作者:
Wirthmueller, Lennart;Zhang, Yan;Parker, Jane E.

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通过核苷酸结合结构域和富含亮氨酸重复序列(NB-LRR)受体识别细胞内的特定病原体分子构成了植物先天免疫的重要层[1]。受体激活触发宿主细胞重编程,涉及基础防御的转录增强和局部程序性细胞死亡[1-3]。然而,对NB-LRR受体的作用位点和作用模式知之甚少。拟南芥Toll/白细胞介素-1(TIR)型NB-LRR受体RPS 4识别细菌III型效应子AvrRps 4 [4]。我们表明,表位标记的RPS 4下,其天然的调控序列分布在内膜和细胞核之间的健康和AvrRPS 4触发的组织。RPS 4积累在核中,介导的一个二分核定位序列(NLS)在其C端,是必要的触发免疫通过真实激活的AvrRps 4在拟南芥或作为一个效应器独立的“解除管制”的受体在烟草。TIR-NB-LRR受体的一个显著保守的特征是它们在对不同病原体的抗性中募集核质基础防御调节剂EDS 1 [5,6]。我们发现,EDS 1是RPS 4信号传导的一个不可或缺的组成部分,它在RPS 4激活的下游发挥作用,但在RPS 4介导的核转录重编程的上游。
Recognition of specific pathogen molecules inside the cell by nucleotide-binding domain and leucine-rich repeat (NB-LRR) receptors constitutes an important layer of innate immunity in plants [1]. Receptor activation triggers host cellular reprogramming involving transcriptional potentiation of basal defenses and localized programmed cell death [1-3]. The sites and modes of action of NB-LRR receptors are, however, poorly understood. Arabidopsis Toll/Interleukin-1 (TIR) type NB-LRR receptor RPS4 recognizes the bacterial type III effector AvrRps4 [4]. We show that epitopetagged RPS4 expressed under its native regulatory sequences distributes between endomembranes and nuclei in healthy and AvrRps4-triggered tissues. RPS4 accumulation in the nucleus, mediated by a bipartite nuclear localization sequence (NLS) at its C terminus, is necessary for triggering immunity through authentic activation by AvrRps4 in Arabidopsis or as an effector-independent "deregulated" receptor in tobacco. A strikingly conserved feature of TIR-NB-LRR receptors is their recruitment of the nucleocytoplasmic basal-defense regulator EDS1 in resistance to diverse pathogens [5, 6]. We find that EDS1 is an indispensable component of RPS4 signaling and that it functions downstream of RPS4 activation but upstream of RPS4-mediated transcriptional reprogramming in the nucleus.