jasmonic-acid and hexanoic-acid

Resistance of tomato (Solanum Lycopersicum) to the fungal pathogen Botrytis cinerea requires complex interplay between hormonal signalling. In this study, we explored the involvement of new oxylipins in the tomato basal and induced response to this necrotroph through the functional analysis of the tomato α-dioxygenase2 (α-DOX2)-deficient mutant divaricata. We also investigated the role of SA in the defence response against this necrotrophic fungus using SA-deficient tomato nahG plants. The plants lacking dioxigenase α-DOX2, which catalyses oxylipins production from fatty acids, were more susceptible to Botrytis, and hexanoic acid-induced resistance (Hx-IR) was impaired; hence α-DOX2 is required for both tomato defence and the enhanced protection conferred by natural inducer hexanoic acid (Hx) against B. cinerea. The divaricata plants accumulated less pathogen-induced callose and presented lower levels of jasmonic acid (JA) and 12-oxo-phytodienoic acid (OPDA) upon infection if compared to the wild type. Glutathion-S-transferase (GST) gene expression decreased and ROS production significantly increased in Botrytis-infected divaricata plants. These results indicate that absence of α-DOX2 influences the hormonal changes, oxidative burst and callose deposition that occur upon Botrytis infection in tomato. The study of SA-deficient nahG tomato plants showed that the plants with low SA levels displayed increased resistance to Botrytis, but were unable to display Hx-IR. This supports the involvement of SA in Hx-IR. NaghG plants displayed reduced callose and ROS accumulation upon infection and an increased GST expression. This reflects a positive relationship between SA and these defensive mechanisms in tomato. Finally, Hx boosted the pathogen-induced callose in nahG plants, suggesting that this priming mechanism is SA-independent. Our results support the involvement of the oxylipins pathway and SA in tomato response to Botrytis, probably through complex crosstalk of the hormonal balance with callose and ROS accumulation, and reinforce the role of the oxidative stress in the outcome of the plant-Botrytis interaction.

Topics: Botrytis; Caproates; Cyclopentanes; Dioxygenases; Disease Resistance; Fatty Acids, Unsaturated; Gene Expression Regulation, Plant; Glucans; Oxylipins; Plant Diseases; Plant Growth Regulators; Plant Proteins; Reactive Oxygen Species; Salicylic Acid; Solanum lycopersicum

In addition to basal defense mechanisms, plants are able to develop enhanced defense mechanisms such as induced resistance (IR) upon appropriate stimulation. We recently described the means by which several carboxylic acids protect Arabidopsis and tomato plants against fungi. In this work, we demonstrate the effectiveness of hexanoic acid (Hx) in the control of Alternaria brown spot (ABS) disease via enhancement of the immune system of Fortune mandarin. The application of 1mM Hx in irrigation water to 2-year-old Fortune plants clearly reduced the incidence of the disease and led to smaller lesions. We observed that several of the most important mechanisms involved in induced resistance were affected by Hx application. Our results demonstrate enhanced callose deposition in infected plants treated with Hx, which suggests an Hx priming mechanism. Plants treated with the callose inhibitor 2-DDG were more susceptible to the fungus. Moreover, polygalacturonase-inhibiting protein (PGIP) gene expression was rapidly and significantly upregulated in treated plants. However, treatment with Hx decreased the levels of reactive oxygen species (ROS) in infected plants. Hormonal and gene analyses revealed that the jasmonic acid (JA) pathway was activated due to a greater accumulation of 12-oxo-phytodienoic acid (OPDA) and JA along with a rapid accumulation of JA-isoleucine (JA-Ile). Furthermore, we observed a more rapid accumulation of abscisic acid (ABA), which could act as a positive regulator of callose deposition. Thus, our results support the hypothesis that both enhanced physical barriers and the JA signaling pathway are involved in hexanoic acid-induced resistance (Hx-IR) to Alternaria alternata.

Topics: Alternaria; Antifungal Agents; Caproates; Citrus; Cyclopentanes; Disease Resistance; Gene Expression Regulation, Plant; Glucans; Oxylipins; Plant Diseases; Plant Growth Regulators

Hexanoic acid-induced resistance (Hx-IR) is effective against several pathogens in tomato plants. Our study of the mechanisms implicated in Hx-IR against Pseudomonas syringae pv. tomato DC3000 suggests that hexanoic acid (Hx) treatment counteracts the negative effect of coronatine (COR) and jasmonyl-isoleucine (JA-Ile) on the salicylic acid (SA) pathway. In Hx-treated plants, an increase in the expression of jasmonic acid carboxyl methyltransferase (JMT) and the SA marker genes PR1 and PR5 indicates a boost in this signalling pathway at the expense of a decrease in JA-Ile. Moreover, Hx treatment potentiates 12-oxo-phytodienoic acid accumulation, which suggests that this molecule might play a role per se in Hx-IR. These results support a positive relationship between the SA and JA pathways in Hx-primed plants. Furthermore, one of the mechanisms of virulence mediated by COR is stomatal re-opening on infection with P. syringae. In this work, we observed that Hx seems to inhibit stomatal opening in planta in the presence of COR, which suggests that, on infection in tomato, this treatment suppresses effector action to prevent bacterial entry into the mesophyll.

Topics: Abscisic Acid; Amino Acids; Biosynthetic Pathways; Caproates; Cyclopentanes; Disease Resistance; Gene Expression Regulation, Plant; Glucans; Indenes; Oxylipins; Plant Diseases; Plant Growth Regulators; Plant Proteins; Plant Stomata; Pseudomonas syringae; Salicylic Acid; Signal Transduction; Solanum lycopersicum; Water

Soil drench treatments with hexanoic acid can effectively protect Arabidopsis plants against Botrytis cinerea through a mechanism based on a stronger and faster accumulation of JA-dependent defenses. Plants impaired in ethylene, salicylic acid, abscisic acid or glutathion pathways showed intact protection by hexanoic acid upon B. cinerea infection. Accordingly, no significant changes in the SA marker gene PR-1 in either the SA or ABA hormone balance were observed in the infected and treated plants. In contrast, the JA signaling pathway showed dramatic changes after hexanoic acid treatment, mainly when the pathogen was present. The impaired JA mutants, jin1-2 and jar1, were unable to display hexanoic acid priming against the necrotroph. In addition, hexanoic acid-treated plants infected with B. cinerea showed priming in the expression of the PDF1.2, PR-4 and VSP1 genes implicated in the JA pathways. Moreover, JA and OPDA levels were primed at early stages by hexanoic acid. Treatments also stimulated increased callose accumulation in response to the pathogen. Although callose accumulation has proved an effective IR mechanism against B. cinerea, it is apparently not essential to express hexanoic acid-induced resistance (HxAc-IR) because the mutant pmr4.1 (callose synthesis defective mutant) is protected by treatment. We recently described how hexanoic acid treatments can protect tomato plants against B. cinerea by stimulating ABA-dependent callose deposition and by priming OPDA and JA-Ile production. We clearly demonstrate here that Hx-IR is a dependent plant species, since this acid protects Arabidopsis plants against the same necrotroph by priming JA-dependent defenses without enhancing callose accumulation.

Topics: Abscisic Acid; Alternaria; Anti-Infective Agents; Arabidopsis; Arabidopsis Proteins; Botrytis; Caproates; Cyclopentanes; Defensins; Endopeptidases; Ethylenes; Gene Expression Regulation, Plant; Glucans; Glutathione; Mutation; Oxylipins; Plant Diseases; Plant Growth Regulators; Plant Immunity; Plant Leaves; Plant Proteins; Plants, Genetically Modified; Salicylic Acid; Signal Transduction