Transcriptional regulation in effector-triggered immunity via NB-LRR resistance genes RPS4 & RRS1

通过 NB-LRR 抗性基因 RPS4 对效应子触发免疫的转录调节

• 批准号: BB/K003550/1
• 负责人: Jonathan Jones
• 金额: $ 40.87万
• 依托单位: University of East Anglia
• 依托单位国家: 英国
• 项目类别: Research Grant
• 财政年份: 2013
• 资助国家: 英国
• 起止时间: 2013 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=BB%2FK003550%2F1
• 关键词: Transcriptional; regulation; effector; triggered; immunity

Crop plants are subject to diseases caused by various microbes that can cause substantial yield losses. Farmers spray agrochemicals to control disease; this is expensive, requires fuel and labour, and leads to soil compaction. It would be preferable for crops to be disease resistant, so that no fungicide applications are required. More knowledge is required to achieve this goal. Breeders use disease resistance (R) genes for crop improvement; more R genes are continuously needed by breeders, because pathogens can evolve to overcome them. R genes confer recognition of pathogen virulence-promoting molecules (so-called "effectors") that contribute to virulence. R gene durability varies; it is likely that more durable R genes recognize the most indispensable effectors for the pathogen. Plant resistance also involves responses to conserved pathogen molecular patterns- "pattern-triggered immunity (PTI)". Although there is overlap in PTI and R gene-mediated resistance responses, the mechanistic link between them is still completely obscure.For durable resistance in our future crops, we need a deep understanding of pathogen virulence and host defence mechanisms. This requires knowledge of the spectrum of host targets of effectors, of how plant R proteins recognize (directly or indirectly) the presence of effectors, and of how upon recognition, defence mechanisms are activated that result in host plant immunity. Plant R proteins resemble mammalian Nod-like receptors (NLRs) that are involved in mammalian innate immunity; for example, Crohn's disease results from a defect in the human NOD2 gene. Mechanisms of NLR signalling are also incompletely understood. NOD2 and NB-LRR proteins carry similar protein modules, with an N-terminal signalling domain, a central nucleotide-binding (NB) domain and a C-terminal leucine-rich repeat (LRR) domain. The proposed work will help us better understand mechanisms of plant resistance. We will study a fascinating disease resistance locus in the model plant Arabidopsis that confers resistance to two distinct bacterial species that cause either bacterial speck or bacterial wilt, and also confers resistance to a fungal pathogen. This locus contains two different NB-LRR R proteins, RRS1 and RPS4, that are transcribed away from each other, and both of which are required for resistance. RPS4 and RRS1 also carry a so-called TIR domain shared with immune receptors of humans and flies. RRS1 has an additional domain (a "WRKY" domain) that has been shown to bind DNA, and that could regulate expression of genes involved in plant defence. RPS4/RRS1 activates defence upon recognizing AvrRps4 effector protein from bacterial speck, or PopP2 effector protein from bacterial wilt, or the fungal pathogen Colletotrichum higginsianum. How this works is still a mystery. - We wish to understand how RPS4/RRS1 activates expression of genes involved in defence upon recognition of AvrRps4 or PopP2. We will investigate the DNA sequences targeted by the DNA binding domain of RRS1, and compare the corresponding genes to the genes that are induced upon RPS4/RRS1 defence activation, and to genes induced during PTI. In this way we will define the direct targets of RPS4/RRS1 and the genes that when activated result in resistance. This will enable us to build up a picture of the chain of events triggered via R proteins that stop the pathogen from growing.- Once we have all the data from these investigations we will be able to propose and test models for what takes place during defence activation, making this system one of the best understood R gene systems; this knowledge will inform approaches to attempting to broaden the recognition capacity of R genes, to thus enhance their utility and durability.

农作物易受由各种微生物引起的疾病的影响，这些疾病可导致显著的产量损失。农民喷洒农用化学品来控制疾病;这是昂贵的，需要燃料和劳动力，并导致土壤压实。作物最好是抗病的，这样就不需要施用杀真菌剂。需要更多的知识来实现这一目标。育种者利用抗病基因来改良作物;育种者不断需要更多的抗病基因，因为病原体可以进化来克服它们。R基因赋予病原体毒力促进分子（所谓的“效应物”）的识别，这些分子有助于毒力。R基因的持久性各不相同;更持久的R基因可能识别病原体最不可或缺的效应子。植物抗性还涉及对保守的病原体分子模式的响应-“模式触发免疫（PTI）"。尽管PTI和R基因介导的抗性反应存在重叠，但它们之间的机制联系仍然完全不清楚，为了使未来作物获得持久的抗性，我们需要深入了解病原菌的毒力和宿主防御机制。这需要了解效应子的宿主靶标谱，植物R蛋白如何识别（直接或间接）效应子的存在，以及识别后如何激活导致宿主植物免疫的防御机制。植物R蛋白类似于参与哺乳动物先天免疫的哺乳动物Nod样受体（NLR）;例如，克罗恩病是由人类NOD 2基因缺陷引起的。NLR信号传导的机制也不完全理解。NOD 2和NB-LRR蛋白携带相似的蛋白模块，具有N-末端信号传导结构域、中央核苷酸结合（NB）结构域和C-末端富含亮氨酸重复（LRR）结构域。这项工作将有助于我们更好地了解植物抗性机制。我们将研究模式植物拟南芥中一个迷人的抗病基因座，该基因座赋予对两种不同细菌的抗性，这两种细菌会导致细菌斑点或细菌枯萎病，并且还赋予对真菌病原体的抗性。该基因座包含两种不同的NB-LRR R蛋白，RRS 1和RPS 4，它们彼此转录，并且两者都是抗性所需的。RPS 4和RRS 1还携带与人类和苍蝇的免疫受体共享的所谓TIR结构域。RRS 1有一个额外的结构域（“WRKY”结构域），已被证明可以结合DNA，并且可以调节参与植物防御的基因的表达。RPS 4/RRS 1在识别来自细菌斑点的AvrRps 4效应蛋白、或来自细菌性枯萎病的PopP 2效应蛋白、或真菌病原体Higginsianum的Colletotrichum后激活防御。这是如何工作的仍然是一个谜。- 我们希望了解RPS 4/RRS 1如何在识别AvrRps 4或PopP 2后激活参与防御的基因的表达。我们将研究RRS 1的DNA结合结构域靶向的DNA序列，并将相应的基因与RPS 4/RRS 1防御激活后诱导的基因以及PTI期间诱导的基因进行比较。通过这种方式，我们将确定RPS 4/RRS 1的直接靶点和激活后导致抗性的基因。这将使我们能够建立一个由R蛋白触发的阻止病原体生长的事件链的图片。-一旦我们从这些调查中获得所有数据，我们将能够提出和测试防御激活过程中发生的模型，使该系统成为最好理解的R基因系统之一;这些知识将为试图扩大R基因识别能力的方法提供信息，从而提高其实用性和耐用性。

项目成果

A Golden Gate Modular Cloning Toolbox for Plants

• DOI: 10.1021/sb4001504
• 发表时间: 2014-11-01
• 期刊: ACS SYNTHETIC BIOLOGY
• 影响因子: 4.7
• 作者: Engler, Carola;Youles, Mark;Marillonnet, Sylvestre
• 通讯作者: Marillonnet, Sylvestre

High-resolution Expression Profiling of Selected Gene Sets during Plant Immune Activation

植物免疫激活过程中选定基因集的高分辨率表达谱

• DOI: 10.1101/775973
• 发表时间: 2019
• 作者: Ding P