Genetic requirements for signaling from an autoactive plant NB-LRR intracellular innate immune receptor.
Genetic requirements for signaling from an autoactive plant NB-LRR intracellular innate immune receptor.
复制标题
来自自动活性植物NB-LRR先天免疫受体的信号传导的遗传要求。
DOI：
10.1371/journal.pgen.1003465
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发表时间：
2013
期刊：
影响因子：
4.5
通讯作者：
Bonardi V
中科院分区：
文献类型：
--
作者：
Roberts M;Tang S;Stallmann A;Dangl JL;Bonardi V
植物通过识别和响应细胞表面和细胞内部的病原体特异性分子来对病原体攻击做出反应。在植物和哺乳动物中，病原体效应物（毒力因子）通过细胞内的核苷酸结合富含亮氨酸重复序列（NB-LRR）传感器蛋白来监测。在这里，我们研究了防御反应的自激活突变体ADR 1-L2，拟南芥卷曲螺旋（CC）-NB-LRR蛋白的遗传要求。ADR 1-L2在几种防御环境中在水杨酸（SA）积累的上游起作用，并且在这种情况下，它可以作为“辅助者”来抑制来自“传感器”NB-LRR的特异性微生物活化信号。这种辅助活性不需要完整的P环。ADR 1-L2和该小NB-LRR家族的两个密切相关的成员中的另一个也是lsd 1突变体中不受调节的失控细胞死亡（rcd）的繁殖所需的。我们在这里证明，在这个特定的背景下，ADR 1-L2功能是P环依赖性的。我们产生了一个自激活的错义突变，ADR 1-L2 D484 V，在一个小的同源基序称为MHD。ADR 1-L2 D848 V的表达导致表现出增加的抗病性和组成型高SA水平的矮化植物。形态表型也需要完整的P环，表明这些ADR 1-L2 D484 V表型反映了该NB-LRR蛋白的典型激活。我们使用ADR 1-L2 D484 V来定义信号传导的遗传要求。来自ADR 1-L2 D484 V的信号传导不需要NADPH氧化酶，并且由EDS 1和AtMC 1负调控。ADR 1-L2 D484 V的转录调控与其表型输出相关;这些输出是SA依赖性和非依赖性的。ADR 1-L2 D484 V活性的遗传要求类似于在LSD 1不存在的情况下最初观察到的调节防御和细胞死亡信号的SA梯度依赖性信号放大的遗传要求。重要的是，ADR 1-L2 D484 V自激活信号传导由EDS 1和SA在可分离但相连的途径中控制。这些数据使我们能够提出一个遗传模型，该模型提供了对SA依赖性反馈调节回路的深入了解，令人惊讶的是，该回路包括ADR 1-L2。植物具有活跃的、可诱导的抗病系统，并且这些反应的诱导部分地依赖于植物抗性蛋白。目前对这些抗性蛋白的理解将它们比作结合核苷酸以激活抗病反应的分子开关。以前的研究表明，激活的抗病性1-样2（ADR 1-L2），一种植物抗病蛋白，在免疫反应中是重要的，但可以在分析的背景下独立于目前认为的典型核苷酸开关激活发挥作用。在这里，我们表明，除了这些以前报道的功能，ADR 1-L2也作为一个典型的，激活的抗病蛋白。我们使用一种自激活突变形式的蛋白质，并表明它促进抗病性。我们发现ADR 1-L2与水杨酸（一种已知对植物抗病性至关重要的激素）在EDS 1依赖的反馈回路中起作用。这项工作使我们能够拓宽对植物抗病蛋白如何发挥作用以产生对病原体的防御的理解。
Plants react to pathogen attack via recognition of, and response to, pathogen-specific molecules at the cell surface and inside the cell. Pathogen effectors (virulence factors) are monitored by intracellular nucleotide-binding leucine-rich repeat (NB-LRR) sensor proteins in plants and mammals. Here, we study the genetic requirements for defense responses of an autoactive mutant of ADR1-L2, an Arabidopsis coiled-coil (CC)-NB-LRR protein. ADR1-L2 functions upstream of salicylic acid (SA) accumulation in several defense contexts, and it can act in this context as a “helper” to transduce specific microbial activation signals from “sensor” NB-LRRs. This helper activity does not require an intact P-loop. ADR1-L2 and another of two closely related members of this small NB-LRR family are also required for propagation of unregulated runaway cell death (rcd) in an lsd1 mutant. We demonstrate here that, in this particular context, ADR1-L2 function is P-loop dependent. We generated an autoactive missense mutation, ADR1-L2D484V, in a small homology motif termed MHD. Expression of ADR1-L2D848V leads to dwarfed plants that exhibit increased disease resistance and constitutively high SA levels. The morphological phenotype also requires an intact P-loop, suggesting that these ADR1-L2D484V phenotypes reflect canonical activation of this NB-LRR protein. We used ADR1-L2D484V to define genetic requirements for signaling. Signaling from ADR1-L2D484V does not require NADPH oxidase and is negatively regulated by EDS1 and AtMC1. Transcriptional regulation of ADR1-L2D484V is correlated with its phenotypic outputs; these outputs are both SA–dependent and –independent. The genetic requirements for ADR1-L2D484V activity resemble those that regulate an SA–gradient-dependent signal amplification of defense and cell death signaling initially observed in the absence of LSD1. Importantly, ADR1-L2D484V autoactivation signaling is controlled by both EDS1 and SA in separable, but linked pathways. These data allows us to propose a genetic model that provides insight into an SA–dependent feedback regulation loop, which, surprisingly, includes ADR1-L2. Plants possess an active, inducible disease resistance system, and induction of these responses depends in part on plant resistance proteins. Present understanding of these resistance proteins likens them to molecular switches that bind nucleotides to activate disease resistance responses. Previously it was shown that Activated Disease Resistance 1-like 2 (ADR1-L2), a plant disease resistance protein, is important in the immune response, but can function in the contexts analysed independently of what is currently considered the canonical nucleotide switch activation. Here, we show that, in addition to these previously reported functions, ADR1-L2 also works as a typical, activated disease resistance protein. We use an autoactive mutant form of the protein and show that it promotes disease resistance. We find that ADR1-L2 works in an EDS1-dependent feedback loop with salicylic acid, a hormone known to be essential for plant disease resistance. This work allows us to broaden the understanding of how plant disease resistance proteins function to generate defense against pathogens.
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影响因子：
5.6
作者：
Bonardi V;Dangl JL
通讯作者：
Dangl JL
影响因子：
11.6
作者：
Bieri, S;Mauch, S;Schulze-Lefert, P
通讯作者：
Schulze-Lefert, P
DOI：
10.1073/pnas.1130421100
发表时间：
2003-05-27
影响因子：
11.1
作者：
Epple, P;Mack, AA;Dangl, JL
通讯作者：
Dangl, JL
影响因子：
7
作者：
Bonardi V;Cherkis K;Nishimura MT;Dangl JL
通讯作者：
Dangl JL
影响因子：
9.5
作者：
Eitas TK;Dangl JL
通讯作者：
Dangl JL