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Development of disease-resistant rice using regulatory components of induced disease resistance.

Takatsuji H - Front Plant Sci (2014)

Bottom Line: This priming effect was similar to that of chemical defense inducers, although the fitness costs were amplified by some environmental factors.WRKY45 is degraded by the ubiquitin-proteasome system, and the dual role of this degradation partly explains the priming effect.The synergistic interaction between SA and cytokinin signaling that activates WRKY45 also likely contributes to the priming effect.

View Article: PubMed Central - PubMed

Affiliation: Disease Resistant Crops Research Unit, Genetically Modified Organism Research Center, National Institute of Agrobiological Sciences Tsukuba, Japan.

ABSTRACT
Infectious diseases cause huge crop losses annually. In response to pathogen attacks, plants activate defense systems that are mediated through various signaling pathways. The salicylic acid (SA) signaling pathway is the most powerful of these pathways. Several regulatory components of the SA signaling pathway have been identified, and are potential targets for genetic manipulation of plants' disease resistance. However, the resistance associated with these regulatory components is often accompanied by fitness costs; that is, negative effects on plant growth and crop yield. Chemical defense inducers, such as benzothiadiazole and probenazole, act on the SA pathway and induce strong resistance to various pathogens without major fitness costs, owing to their 'priming effect.' Studies on how benzothiadiazole induces disease resistance in rice have identified WRKY45, a key transcription factor in the branched SA pathway, and OsNPR1/NH1. Rice plants overexpressing WRKY45 were extremely resistant to rice blast disease caused by the fungus Magnaporthe oryzae and bacterial leaf blight disease caused by Xanthomonas oryzae pv. oryzae (Xoo), the two major rice diseases. Disease resistance is often accompanied by fitness costs; however, WRKY45 overexpression imposed relatively small fitness costs on rice because of its priming effect. This priming effect was similar to that of chemical defense inducers, although the fitness costs were amplified by some environmental factors. WRKY45 is degraded by the ubiquitin-proteasome system, and the dual role of this degradation partly explains the priming effect. The synergistic interaction between SA and cytokinin signaling that activates WRKY45 also likely contributes to the priming effect. With a main focus on these studies, I review the current knowledge of SA-pathway-dependent defense in rice by comparing it with that in Arabidopsis, and discuss potential strategies to develop disease-resistant rice using signaling components.

No MeSH data available.


Related in: MedlinePlus

Effects of priming on induced disease resistance. (A) In untreated wild-type plants, activation of defense reactions is slow and/or weak to counteract pathogens. By contrast, constitutive defense activation imposes fitness costs on plants. Chemical defense inducers such as BTH prime plants for rapid and/or strong defense reactions upon pathogen infection, thereby conferring plants with disease resistance without major fitness costs. (B) Overexpression of NPR1 (Arabidopsis) or WRKY45 (rice) mimics priming by BTH. (C) UPS degradation of NPR1 (Arabidopsis) or WRKY45 (rice) suppresses basal defense levels in the absence of pathogens, and enhances defense levels upon pathogen infection, possibly contributing to the priming effect. (D) Environmental factors increase basal levels of WRKY45-dependent defense, leading to higher fitness costs.
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Figure 1: Effects of priming on induced disease resistance. (A) In untreated wild-type plants, activation of defense reactions is slow and/or weak to counteract pathogens. By contrast, constitutive defense activation imposes fitness costs on plants. Chemical defense inducers such as BTH prime plants for rapid and/or strong defense reactions upon pathogen infection, thereby conferring plants with disease resistance without major fitness costs. (B) Overexpression of NPR1 (Arabidopsis) or WRKY45 (rice) mimics priming by BTH. (C) UPS degradation of NPR1 (Arabidopsis) or WRKY45 (rice) suppresses basal defense levels in the absence of pathogens, and enhances defense levels upon pathogen infection, possibly contributing to the priming effect. (D) Environmental factors increase basal levels of WRKY45-dependent defense, leading to higher fitness costs.

Mentions: Defense responses usually have fitness costs, which reflect the tradeoff between disease resistance and plant growth. The tradeoff is believed to be a consequence of resource allocation to defensive compounds and/or the toxicity of the defensive compounds themselves (Heil and Baldwin, 2002). Plants presumably have evolved inducible defense mechanisms to circumvent such negative effects of defense responses. Consistent with this idea, Arabidopsis mutants with constitutively activated defense responses, such as cpr (constitutive expressor of PR genes), in which the SA pathway is constitutively activated (Clarke et al., 2000), show severe growth defects (Figure 1A).


Development of disease-resistant rice using regulatory components of induced disease resistance.

Takatsuji H - Front Plant Sci (2014)

Effects of priming on induced disease resistance. (A) In untreated wild-type plants, activation of defense reactions is slow and/or weak to counteract pathogens. By contrast, constitutive defense activation imposes fitness costs on plants. Chemical defense inducers such as BTH prime plants for rapid and/or strong defense reactions upon pathogen infection, thereby conferring plants with disease resistance without major fitness costs. (B) Overexpression of NPR1 (Arabidopsis) or WRKY45 (rice) mimics priming by BTH. (C) UPS degradation of NPR1 (Arabidopsis) or WRKY45 (rice) suppresses basal defense levels in the absence of pathogens, and enhances defense levels upon pathogen infection, possibly contributing to the priming effect. (D) Environmental factors increase basal levels of WRKY45-dependent defense, leading to higher fitness costs.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4230042&req=5

Figure 1: Effects of priming on induced disease resistance. (A) In untreated wild-type plants, activation of defense reactions is slow and/or weak to counteract pathogens. By contrast, constitutive defense activation imposes fitness costs on plants. Chemical defense inducers such as BTH prime plants for rapid and/or strong defense reactions upon pathogen infection, thereby conferring plants with disease resistance without major fitness costs. (B) Overexpression of NPR1 (Arabidopsis) or WRKY45 (rice) mimics priming by BTH. (C) UPS degradation of NPR1 (Arabidopsis) or WRKY45 (rice) suppresses basal defense levels in the absence of pathogens, and enhances defense levels upon pathogen infection, possibly contributing to the priming effect. (D) Environmental factors increase basal levels of WRKY45-dependent defense, leading to higher fitness costs.
Mentions: Defense responses usually have fitness costs, which reflect the tradeoff between disease resistance and plant growth. The tradeoff is believed to be a consequence of resource allocation to defensive compounds and/or the toxicity of the defensive compounds themselves (Heil and Baldwin, 2002). Plants presumably have evolved inducible defense mechanisms to circumvent such negative effects of defense responses. Consistent with this idea, Arabidopsis mutants with constitutively activated defense responses, such as cpr (constitutive expressor of PR genes), in which the SA pathway is constitutively activated (Clarke et al., 2000), show severe growth defects (Figure 1A).

Bottom Line: This priming effect was similar to that of chemical defense inducers, although the fitness costs were amplified by some environmental factors.WRKY45 is degraded by the ubiquitin-proteasome system, and the dual role of this degradation partly explains the priming effect.The synergistic interaction between SA and cytokinin signaling that activates WRKY45 also likely contributes to the priming effect.

View Article: PubMed Central - PubMed

Affiliation: Disease Resistant Crops Research Unit, Genetically Modified Organism Research Center, National Institute of Agrobiological Sciences Tsukuba, Japan.

ABSTRACT
Infectious diseases cause huge crop losses annually. In response to pathogen attacks, plants activate defense systems that are mediated through various signaling pathways. The salicylic acid (SA) signaling pathway is the most powerful of these pathways. Several regulatory components of the SA signaling pathway have been identified, and are potential targets for genetic manipulation of plants' disease resistance. However, the resistance associated with these regulatory components is often accompanied by fitness costs; that is, negative effects on plant growth and crop yield. Chemical defense inducers, such as benzothiadiazole and probenazole, act on the SA pathway and induce strong resistance to various pathogens without major fitness costs, owing to their 'priming effect.' Studies on how benzothiadiazole induces disease resistance in rice have identified WRKY45, a key transcription factor in the branched SA pathway, and OsNPR1/NH1. Rice plants overexpressing WRKY45 were extremely resistant to rice blast disease caused by the fungus Magnaporthe oryzae and bacterial leaf blight disease caused by Xanthomonas oryzae pv. oryzae (Xoo), the two major rice diseases. Disease resistance is often accompanied by fitness costs; however, WRKY45 overexpression imposed relatively small fitness costs on rice because of its priming effect. This priming effect was similar to that of chemical defense inducers, although the fitness costs were amplified by some environmental factors. WRKY45 is degraded by the ubiquitin-proteasome system, and the dual role of this degradation partly explains the priming effect. The synergistic interaction between SA and cytokinin signaling that activates WRKY45 also likely contributes to the priming effect. With a main focus on these studies, I review the current knowledge of SA-pathway-dependent defense in rice by comparing it with that in Arabidopsis, and discuss potential strategies to develop disease-resistant rice using signaling components.

No MeSH data available.


Related in: MedlinePlus