The strobilurin class of fungicides comprises a variety of synthetic plant-protecting compounds with broad-spectrum antifungal activity. In the present study, we demonstrate that a strobilurin fungicide, F 500 (Pyraclostrobin), enhances the resistance of tobacco (Nicotiana tabacum cv Xanthi nc) against infection by either tobacco mosaic virus (TMV) or the wildfire pathogenPseudomonas syringae pv tabaci. F 500 was also active at enhancing TMV resistance in NahGtransgenic tobacco plants unable to accumulate significant amounts of the endogenous inducer of enhanced disease resistance, salicylic acid (SA). This finding suggests that F 500 enhances TMV resistance in tobacco either by acting downstream of SA in the SA signaling mechanism or by functioning independently of SA. The latter assumption is the more likely because in infiltrated leaves, F 500 did not cause the accumulation of SA-inducible pathogenesis-related (PR)-1 proteins that often are used as conventional molecular markers for SA-induced disease resistance. However, accumulation of PR-1 proteins and the associated activation of the PR-1 genes were elicited upon TMV infection of tobacco leaves and both these responses were induced more rapidly in F 500-pretreated plants than in the water-pretreated controls. Taken together, our results suggest that F 500, in addition to exerting direct antifungal activity, may also protect plants by priming them for potentiated activation of subsequently pathogen-induced cellular defense responses.
SummaryInfection of one leaf of cucumber (Cucumis sativa) plants can render other leaves resistant to various pathogens. This so-called systemic acquired resistance (SAR) can be functionally mimicked by certain chemicals. All these treatments enhanced expression of a gene encoding a novel proline-rich protein (PRP1) which has C-terminal repetitive sequences containing an unusually high amount of lysine and arginine residues. Antibodies raised against a synthetic peptide derived from four of the repetitive sequences cross-reacted mainly with a cell wall polypeptide of an apparent MW of 8 kDa. The protein accumulated upon SAR induction, though it does not appear to take part in oxidative protein cross-linking, at least in the hypocotyl tissue. The synthetic peptide derived from the repetitive sequences was able to polymerize orthosilicic acid to insoluble silica, a property not resulting directly from the primary protein sequence, but rather from the high positive charge density. Our results suggest that during induction of SAR, the synthesis of a strongly cationic PRP prepares the cell walls for enhanced silica deposition which is known to participate in cell wall reinforcement, localized at the site of attempted penetration of fungi into epidermal cells. Constitutive accumulation of related PRPs may function in silica deposition during certain developmental stages, a process important for various physiological functions of green plants.
Inoculation of soybean (Glycine max [L.] Merr.) cell-suspension cultures with avirulent bacteria results in a salicylic acid (SA)-controlled programmed cell death (pcd). To unravel the nature of the SA-dependent step in pcd, a screening procedure for complementing compounds was performed. Diverse chemicals that are well known as activating ligands for orphan receptors in animals, particularly receptors of the PPAR (peroxisome proliferator-activated receptor) subfamily, were found to be active. These include the compounds WY-14643, flufenamic acid, LY-171883, tolbutamide, indomethacin and clofibrate. A new marker gene (DD-CA9) from soybean that is induced in the hypersensitive reaction by SA and by PPAR ligands was isolated by differential display, and showed homology to antifungal lectins. In plants, SA is also involved in a signal transduction pathway leading to systemic acquired resistance (SAR). The PPAR ligands which act on the pcd pathway for plant resistance induce a beta-1,3-glucanase gene in soybean at high concentrations but do not induce marker genes of the SAR pathway such as the PR-1 gene in tobacco or Arabidopsis. Thus SA seems to act on two independent plant defence pathways that can now be separately activated by synthetic compounds. We propose a model for the control of pcd by SA in soybean, in which SA induces the transcription of (novel) genes required for the final completion of the cell death program.
Soybean (Glycine max [L.] Merr.) cell suspension cultures (cv. Williams 82) inoculated with the pathogenic bacteria Pseudomonas syringae pv. glycinea respond with a hypersensitive reaction (HR) when the bacteria express the avirulence gene avrA. A mRNA differential display was established for this system to allow the identification of genes induced during the HR. Six PCR-fragments (DD1-DD6) from the differential display analysis were identified, which are induced during the HR. Database searches revealed that the fragment DD1 encodes chalcone isomerase and DD2 was identified as ubiquitin. The fragment DD3 shares significant homology to the signalling molecule 14-3-3. The partial DD4 product is homologous to the enhancer of rudimentary from Drosophila and an uncharacterized homologue of it from Arabidopsis. The fragment DD5 is similar to glucose-6-phosphate dehydrogenase which provides NADPH to the cell. The PCR-product DD6 seems to be a new leucine-rich-repeat disease resistance gene from soybean, which is significantly induced during the HR. All of the identified genes are clearly induced during a HR in infected plants of the same cultivar, indicating that results from the cell culture model system can be transferred to intact plants. These studies show that complex mRNA differential display is a powerful tool to identify new induced gene in plant-pathogen interactions.
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.