Plants have the ability to acquire an enhanced level of resistance to pathogen attack after being exposed to specific biotic stimuli. In Arabidopsis, nonpathogenic, root-colonizing Pseudomonas fluorescens bacteria trigger an induced systemic resistance (ISR) response against infection by the bacterial leaf pathogen P. syringae pv tomato. In contrast to classic, pathogen-induced systemic acquired resistance (SAR), this rhizobacteria-mediated ISR response is independent of salicylic acid accumulation and pathogenesis-related gene activation. Using the jasmonate response mutant jar1 , the ethylene response mutant etr1 , and the SAR regulatory mutant npr1 , we demonstrate that signal transduction leading to P. fluorescens WCS417r-mediated ISR requires responsiveness to jasmonate and ethylene and is dependent on NPR1. Similar to P. fluorescens WCS417r, methyl jasmonate and the ethylene precursor 1-aminocyclopropane-1-carboxylate were effective in inducing resistance against P. s. tomato in salicylic acid-nonaccumulating NahG plants. Moreover, methyl jasmonate-induced protection was blocked in jar1 , etr1 , and npr1 plants, whereas 1-aminocyclopropane-1-carboxylate-induced protection was affected in etr1 and npr1 plants but not in jar1 plants. Hence, we postulate that rhizobacteria-mediated ISR follows a novel signaling pathway in which components from the jasmonate and ethylene response are engaged successively to trigger a defense reaction that, like SAR, is regulated by NPR1. We provide evidence that the processes downstream of NPR1 in the ISR pathway are divergent from those in the SAR pathway, indicating that NPR1 differentially regulates defense responses, depending on the signals that are elicited during induction of resistance. INTRODUCTIONPlants of which the roots have been colonized by selected strains of nonpathogenic fluorescent Pseudomonas spp develop an enhanced level of protection against pathogen attack (reviewed in van Loon et al., 1998). Strain WCS417r of P. fluorescens is a biological control strain that has been shown to trigger an induced systemic resistance (ISR) response in several plant species, including carnation (van Peer et al., 1991), radish (Leeman et al., 1995), tomato (Duijff et al., 1996), and Arabidopsis (Pieterse et al., 1996). In Arabidopsis, P. fluorescens WCS417r-mediated ISR has been demonstrated against the bacterial leaf pathogen P. syringae pv tomato , the fungal root pathogen Fusarium oxysporum f sp raphani (Pieterse et al., 1996;van Wees et al., 1997), and the fungal leaf pathogen Peronospora parasitica (J. Ton and C.M.J. Pieterse, unpublished data), indicating that this type of biologically induced resistance is effective against different types of pathogens.ISR-inducing rhizobacteria show host specificity in regard to eliciting resistance (Leeman et al., 1995;van Wees et al., 1997), which indicates that specific recognition between protective bacteria and the plant is a prerequisite for the activation of the signaling cascade leading to ISR. The downstream signaling event...
Plants have the ability to acquire an enhanced level of resistance to pathogen attack after being exposed to specific biotic stimuli. In Arabidopsis, nonpathogenic, root-colonizing Pseudomonas fluorescens bacteria trigger an induced systemic resistance (ISR) response against infection by the bacterial leaf pathogen P. syringae pv tomato. In contrast to classic, pathogen-induced systemic acquired resistance (SAR), this rhizobacteria-mediated ISR response is independent of salicylic acid accumulation and pathogenesis-related gene activation. Using the jasmonate response mutant jar1 , the ethylene response mutant etr1 , and the SAR regulatory mutant npr1 , we demonstrate that signal transduction leading to P. fluorescens WCS417r-mediated ISR requires responsiveness to jasmonate and ethylene and is dependent on NPR1. Similar to P. fluorescens WCS417r, methyl jasmonate and the ethylene precursor 1-aminocyclopropane-1-carboxylate were effective in inducing resistance against P. s. tomato in salicylic acid-nonaccumulating NahG plants. Moreover, methyl jasmonate-induced protection was blocked in jar1 , etr1 , and npr1 plants, whereas 1-aminocyclopropane-1-carboxylate-induced protection was affected in etr1 and npr1 plants but not in jar1 plants. Hence, we postulate that rhizobacteria-mediated ISR follows a novel signaling pathway in which components from the jasmonate and ethylene response are engaged successively to trigger a defense reaction that, like SAR, is regulated by NPR1. We provide evidence that the processes downstream of NPR1 in the ISR pathway are divergent from those in the SAR pathway, indicating that NPR1 differentially regulates defense responses, depending on the signals that are elicited during induction of resistance. INTRODUCTIONPlants of which the roots have been colonized by selected strains of nonpathogenic fluorescent Pseudomonas spp develop an enhanced level of protection against pathogen attack (reviewed in van Loon et al., 1998). Strain WCS417r of P. fluorescens is a biological control strain that has been shown to trigger an induced systemic resistance (ISR) response in several plant species, including carnation (van Peer et al., 1991), radish (Leeman et al., 1995), tomato (Duijff et al., 1996), and Arabidopsis (Pieterse et al., 1996). In Arabidopsis, P. fluorescens WCS417r-mediated ISR has been demonstrated against the bacterial leaf pathogen P. syringae pv tomato , the fungal root pathogen Fusarium oxysporum f sp raphani (Pieterse et al., 1996;van Wees et al., 1997), and the fungal leaf pathogen Peronospora parasitica (J. Ton and C.M.J. Pieterse, unpublished data), indicating that this type of biologically induced resistance is effective against different types of pathogens.ISR-inducing rhizobacteria show host specificity in regard to eliciting resistance (Leeman et al., 1995;van Wees et al., 1997), which indicates that specific recognition between protective bacteria and the plant is a prerequisite for the activation of the signaling cascade leading to ISR. The downstream signaling event...
Enhanced ethylene production is an early response of plants to pathogen attack and has been associated with both resistance and susceptibility to disease. Tobacco plants were transformed with the mutant etr1-1 gene from Arabidopsis, conferring dominant ethylene insensitivity. Besides lacking known ethylene responses, these transformants (Tetr) did not slow growth when contacting neighboring plants, hardly expressed defense-related basic pathogenesisrelated proteins, and developed spontaneous stem browning. Whereas hypersensitive resistance to tobacco mosaic virus was unimpaired, Tetr plants had lost nonhost resistance against normally nonpathogenic soil-borne fungi.
Root colonization of Arabidopsis thaliana by the nonpathogenic, rhizosphere-colonizing, biocontrol bacterium Pseudomonas fluorescens WCS417r has been shown to elicit induced systemic resistance (ISR) against Pseudomonas syringae pv. tomato (Pst). The ISR response differs from the pathogen-inducible systemic acquired resistance (SAR) response in that ISR is independent of salicylic acid and not associated with pathogenesis-related proteins. Several ethylene-response mutants were tested and showed essentially normal symptoms of Pst infection. ISR was abolished in the ethylene-insensitive mutant etr1-1, whereas SAR was unaffected. Similar results were obtained with the ethylene-insensitive mutants ein2 through ein7, indicating that the expression of ISR requires the complete signal-transduction pathway of ethylene known so far. The induction of ISR by WCS417r was not accompanied by increased ethylene production in roots or leaves, nor by increases in the expression of the genes encoding the ethylene biosynthetic enzymes 1-aminocyclopropane-1-carboxylic (ACC) synthase and ACC oxidase. The eir1 mutant, displaying ethylene insensitivity in the roots only, did not express ISR upon application of WCS417r to the roots, but did exhibit ISR when the inducing bacteria were infiltrated into the leaves. These results demonstrate that, for the induction of ISR, ethylene responsiveness is required at the site of application of inducing rhizobacteria.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.