scholarly journals WRKY Transcription Factors Shared by BTH-Induced Resistance and NPR1-Mediated Acquired Resistance Improve Broad-Spectrum Disease Resistance in Wheat

2020 ◽  
Vol 33 (3) ◽  
pp. 433-443 ◽  
Author(s):  
Huanpeng Li ◽  
Jiaojiao Wu ◽  
Xiaofeng Shang ◽  
Miaomiao Geng ◽  
Jing Gao ◽  
...  

In Arabidopsis, both pathogen invasion and benzothiadiazole (BTH) treatment activate the nonexpresser of pathogenesis-related genes 1 (NPR1)-mediated systemic acquired resistance, which provides broad-spectrum disease resistance to secondary pathogen infection. However, the BTH-induced resistance in Triticeae crops of wheat and barley seems to be accomplished through an NPR1-independent pathway. In the current investigation, we applied transcriptome analysis on barley transgenic lines overexpressing wheat wNPR1 (wNPR1-OE) and knocking down barley HvNPR1 (HvNPR1-Kd) to reveal the role of NPR1 during the BTH-induced resistance. Most of the previously designated barley chemical-induced (BCI) genes were upregulated in an NPR1-independent manner, whereas the expression levels of several pathogenesis-related (PR) genes were elevated upon BTH treatment only in wNPR1-OE. Two barley WRKY transcription factors, HvWRKY6 and HvWRKY70, were predicted and further validated as key regulators shared by the BTH-induced resistance and the NPR1-mediated acquired resistance. Wheat transgenic lines overexpressing HvWRKY6 and HvWRKY70 showed different degrees of enhanced resistance to Puccinia striiformis f. sp. tritici pathotype CYR32 and Blumeria graminis f. sp. tritici pathotype E20. In conclusion, the transcriptional changes of BTH-induced resistance in barley were initially profiled, and the identified key regulators would be valuable resources for the genetic improvement of broad-spectrum disease resistance in wheat. [Formula: see text] Copyright © 2020 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

2016 ◽  
Vol 29 (12) ◽  
pp. 977-989 ◽  
Author(s):  
Xiaodong Wang ◽  
Baoju Yang ◽  
Kun Li ◽  
Zhensheng Kang ◽  
Dario Cantu ◽  
...  

In Arabidopsis, NPR1 is a key transcriptional coregulator of systemic acquired resistance. Upon pathogen challenge, NPR1 translocates from the cytoplasm to the nucleus, in which it interacts with TGA-bZIP transcription factors to activate the expression of several pathogenesis-related (PR) genes. In a screen of a yeast two-hybrid library from wheat leaves infected with Puccinia striiformis f. sp. tritici, we identified a conserved rust protein that interacts with wheat NPR1 and named it PNPi (for Puccinia NPR1 interactor). PNPi interacts with the NPR1/NIM1-like domain of NPR1 via its C-terminal DPBB_1 domain. Using bimolecular fluorescence complementation assays, we detected the interaction between PNPi and wheat NPR1 in the nucleus of Nicotiana benthamiana protoplasts. A yeast three-hybrid assay showed that PNPi interaction with NPR1 competes with the interaction between wheat NPR1 and TGA2.2. In barley transgenic lines overexpressing PNPi, we observed reduced induction of multiple PR genes in the region adjacent to Pseudomonas syringae pv. tomato DC3000 infection. Based on these results, we hypothesize that PNPi has a role in manipulating wheat defense response via its interactions with NPR1.


2018 ◽  
Author(s):  
Yun Chu Chen ◽  
Eric C. Holmes ◽  
Jakub Rajniak ◽  
Jung-Gun Kim ◽  
Sandy Tang ◽  
...  

AbstractSystemic acquired resistance (SAR) is a global response in plants induced at the site of infection that leads to long-lasting and broad-spectrum disease resistance at distal, uninfected tissues. Despite the importance of this priming mechanism, the identity of the mobile defense signal that moves systemically throughout plants to initiate SAR has remained elusive. In this paper, we describe a new metabolite, N-hydroxy-pipecolic acid (N-OH-Pip), and provide evidence that this molecule is a mobile signal that plays a central role in initiating SAR signal transduction in Arabidopsis thaliana. We demonstrate that FLAVIN-DEPENDENT MONOOXYGENASE 1 (FMO1), a key regulator of SAR-associated defense priming, can synthesize N-OH-Pip from pipecolic acid in planta, and exogenously applied N-OH-PIP moves systemically in Arabidopsis and can rescue the SAR-deficiency of fmo1 mutants. We also demonstrate that N-OH-Pip treatment causes systemic changes in the expression of pathogenesis-related genes and metabolic pathways throughout the plant, and enhances resistance to a bacterial pathogen. This work provides new insight into the chemical nature of a mobile signal for SAR and also suggests that the N-OH-Pip pathway is a promising target for metabolic engineering to enhance disease resistance.


2005 ◽  
Vol 15 (3) ◽  
pp. 518-529 ◽  
Author(s):  
Andrea B. da Rocha ◽  
Ray Hammerschmidt

A major challenge facing horticultural crop production is the need to provide field and postharvest disease control measures that help maintain high quality plant products. Producers and consumers also expect high quality produce with minimal or no pesticide residues and competitive prices. The chemical management of disease is further complicated by the development of fungicide resistance in many important pathogens. Because of these concerns, an alternative or complementary approach is the use of disease resistance inducers that activate the natural defenses of the plant. Induced disease resistance in plants has been studied in many different pathosystems for nearly a century. Resistance to plant disease can be induced systemically by prior infection with pathogens, by certain non-pathogenic microbes that colonize the surface of roots and leaves, or by chemicals. The application of resistance inducers should protect plants through the induction of defenses that are effective against a broad spectrum of pathogens. Over the last few years, a number of materials that could potentially be used as inducers of resistance in horticultural crops have been identified. Some of these materials are already commercially available. Although induced resistance is known to provide a broad spectrum of disease suppression, it may not be a complete solution because variation in the efficacy of disease resistance induction has been observed. The variation in the response may be dependent on the plant species and even cultivars, as well as variability in the spectrum of pathogens that resistance can be induced against. Induction of resistance depends on the activation of biochemical processes that are triggered in the plant, and therefore a lag time between treatment and expression of resistance occurs. This lag effect may limit the practical application of disease resistance inducers. Since the efficacy of the inducers also depends on the part of the plant that was treated, the product delivery (i.e., how the inducers would be applied in order to optimize their action) is another factor to be considered. Some studies have shown that there may be side effects on growth or yield characteristics when certain inducers are used. Understanding the biochemical interactions occurring between plants, pathogens and the inducers will provide information that may be useful for the optimization of this new approach on disease control. Approaches to integrate induced resistance with other management practices need to be investigated as a means to aid the development of sustainable disease management programs that are effective as well as economically and environmentally sound.


1998 ◽  
Vol 11 (7) ◽  
pp. 643-658 ◽  
Author(s):  
Shericca W. Morris ◽  
Bernard Vernooij ◽  
Somkiat Titatarn ◽  
Mark Starrett ◽  
Steve Thomas ◽  
...  

Systemic acquired resistance (SAR) is a widely distributed plant defense system that confers broad-spectrum disease resistance and is accompanied by coordinate expression of the so-called SAR genes. This type of resistance and SAR gene expression can be mimicked with chemical inducers of resistance. Here, we report that chemical inducers of resistance are active in maize. Chemical induction increases resistance to downy mildew and activates expression of the maize PR-1 and PR-5 genes. These genes are also coordinately activated by pathogen infection and function as indicators of the defense reaction. Specifically, after pathogen infection, the PR-1 and PR-5 genes are induced more rapidly and more strongly in an incompatible than in a compatible interaction. In addition, we show that monocot lesion mimic plants also express these defense-related genes and that they have increased levels of salicylic acid after lesions develop, similar to pathogen-infected maize plants. The existence of chemically inducible disease resistance and PR-1 and PR-5 gene expression in maize indicates that maize is similar to dicots in many aspects of induced resistance. This reinforces the notion of an ancient plant-inducible defense pathway against pathogen attack that is shared between monocots and dicots.


2020 ◽  
Vol 71 (22) ◽  
pp. 7393-7404
Author(s):  
Xiaoxiao Liu ◽  
Hui Liu ◽  
Jingjing He ◽  
Siyuan Zhang ◽  
Hui Han ◽  
...  

Abstract Plants have evolved an innate immune system to protect themselves from pathogen invasion with the help of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors, though the mechanisms remain largely undefined. RIN13 (RPM1-interacting protein 13) was previously reported to enhance disease resistance, and suppress RPM1 (a CNL-type NLR)-mediated hypersensitive response in Arabidopsis via an as yet unknown mechanism. Here, we show that RIN13 is a nuclear-localized protein, and functions therein. Overexpression of RIN13 leads to autoimmunity with high accumulation of salicylic acid (SA), constitutive expression of pathogenesis-related genes, enhanced resistance to a virulent pathogen, and dwarfism. In addition, genetic and transcriptome analyses show that SA-dependent and SA-independent pathways are both required for RIN13-mediated disease resistance, with the EDS1/PAD4 complex as an integration point. RIN13-induced dwarfism was rescued completely by either the pad4-1 or the eds1-2 mutant but partially by snc1-r1, a mutant of the TNL gene SNC1, suggesting the involvement of EDS1/PAD4 and SNC1 in RIN13 functioning. Furthermore, transient expression assays indicated that RIN13 promotes the nuclear accumulation of PAD4. Collectively, our study uncovered a signaling pathway whereby SNC1 and EDS1/PAD4 act together to modulate RIN13-triggered plant defense responses.


2018 ◽  
Vol XI ◽  
pp. 21-30
Author(s):  
Emilia Wilmowicz ◽  
Agata Kućko ◽  
Jan Kopcewicz

This paper presents a comprehensive study on the mechanisms of tree responses to pathogens. We describe natural resistance concerning the presence of different types of barriers protecting plants from invasion and also give them strength after a pathogen attack. We put emphasis on induced resistance functioning both locally and systemically and involvement of phytohormones signaling networks. Systemic acquired resistance (SAR) involved the action of salicylic acid and H202 and accumulation of pathogenesis-related proteins. In turn, jasmonates and ethylene are signaling molecules in the induced resistance (SIR). All these substances play a crucial role in the forest management and can be applied in the tree protection strategies based on the natural and synthetic active compounds.


2020 ◽  
Vol 145 ◽  
pp. 01038
Author(s):  
Pan Wang ◽  
Meiqin Xiang

Salicylic acid (SA) is considered to be an endogenous signal molecule in plants, and it is related to many resistances in plants. In Arabidopsis, Non-expressor of pathogenesis-related gene1 (NPR1) mediates the expression of pathogenesis-related genes (PRs) and systemic acquired resistance (SAR) induced by SA. NPR1 is a key factor in SA signaling pathway, and the research shows that NPR1, NPR3 and NPR4 play a key role in SA mediated plant disease resistance. In this review, the interaction between NPR and transcription factors is discussed, and we also describe the progress of NPR in SA mediated SAR signal transduction pathway, likewise, we introduce the relationship between NPR1 and its paralogues NPR3/NPR4. This paper analyzes the research prospect of NPR as the intersection of multiple signal paths.


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