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Systemic Acquired Resistance-Mediated Control of Pine Wilt Disease by Foliar Application With Methyl Salicylate.

ABSTRACT: Pine wilt disease (PWD), caused by the pinewood nematode, is the most destructive disease in pine forest ecosystems worldwide. Extensive research has been done on PWD, but effective disease management is yet to be devised. Generally, plants can resist pathogen attack via a combination of constitutive and inducible defenses. Systemic acquired resistance (SAR) is an inducible defense that occurs by the localized infection of pathogens or treatment with elicitors. To manage PWD by SAR in pine trees, we tested previously known 12 SAR elicitors. Among them, methyl salicylate (MeSA) was found to induce resistance against PWD in Pinus densiflora seedlings. In addition, the foliar applications of the dispersible concentrate-type formulation of MeSA (MeSA 20 DC) and the emulsifiable concentrate-type formulation of MeSA (MeSA 20 EC) resulted in significantly reduced PWD in pine seedlings. In the field test using 10-year-old P. densiflora trees, MeSA 20 DC showed a 60% decrease in the development of PWD. Also, MeSA 20 EC gave the best results when applied at 0.1 mM concentration 2 and 1 weeks before pinewood nematode (PWN) inoculation in pine seedlings. qRT-PCR analysis confirmed that MeSA induced the expression of defense-related genes, indicating that MeSA can inhibit and delay the migration and reproduction of PWN in pine seedlings by modulating gene expression. These results suggest that foliar application of MeSA could reduce PWD incidence by inducing resistance and provide an economically feasible alternative to trunk-injection agents for PWD management.

SUBMITTER: Jeon HW

PROVIDER: S-EPMC8767056 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Genome-wide microarray analyses revealed that during biological activation of systemic acquired resistance (SAR) in Arabidopsis, the transcript levels of several hundred plant genes were consistently up- (SAR(+) genes) or down-regulated (SAR(-) genes) in systemic, non-inoculated leaf tissue. This transcriptional reprogramming fully depended on the SAR regulator FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1). Functional gene categorization showed that genes associated with salicylic acid (SA)-associated defenses, signal transduction, transport, and the secretory machinery are overrepresented in the group of SAR(+) genes, and that the group of SAR(-) genes is enriched in genes activated via the jasmonate (JA)/ethylene (ET)-defense pathway, as well as in genes associated with cell wall remodeling and biosynthesis of constitutively produced secondary metabolites. This suggests that SAR-induced plants reallocate part of their physiological activity from vegetative growth towards SA-related defense activation. Alignment of the SAR expression data with other microarray information allowed us to define three clusters of SAR(+) genes. Cluster I consists of genes tightly regulated by SA. Cluster II genes can be expressed independently of SA, and this group is moderately enriched in H2O2- and abscisic acid (ABA)-responsive genes. The expression of the cluster III SAR(+) genes is partly SA-dependent. We propose that SA-independent signaling events in early stages of SAR activation enable the biosynthesis of SA and thus initiate SA-dependent SAR signaling. Both SA-independent and SA-dependent events tightly co-operate to realize SAR. SAR(+) genes function in the establishment of diverse resistance layers, in the direct execution of resistance against different (hemi-)biotrophic pathogen types, in suppression of the JA- and ABA-signaling pathways, in redox homeostasis, and in the containment of defense response activation. Our data further indicated that SAR-associated defense priming can be realized by partial pre-activation of particular defense pathways.

Project description:For the treatment of foliar diseases of cereals, fungicides may be applied as foliar sprays or systemic seed treatments which are translocated to leaves. Little research has been done to assess the resistance risks associated with foliar-acting systemic seed treatments when used alone or in combination with foliar sprays, even though both types of treatment may share the same mode of action. It is therefore unknown to what extent adding a systemic seed treatment to a foliar spray programme poses an additional resistance risk and whether in the presence of a seed treatment additional resistance management strategies (such as limiting the total number of treatments) are necessary to limit the evolution of fungicide-resistance. A mathematical model was developed to simulate an epidemic and the resistance evolution of Zymoseptoria tritici on winter wheat, which was used to compare different combinations of seed and foliar treatments by calculating the fungicide effective life, i.e. the number of years before effective disease control is lost to resistance. A range of parameterizations for the seed treatment fungicide and different fungicide uptake models were compared. Despite the different parameterizations, the model consistently predicted the same trends in that i) similar levels of efficacy delivered either by a foliar-acting seed treatment, or a foliar application, resulted in broadly similar resistance selection, ii) adding a foliar-acting seed treatment to a foliar spray programme increased resistance selection and usually decreased effective life, and iii) splitting a given total dose-by adding a seed treatment to foliar treatments, but decreasing dose per treatment-gave effective lives that were the same as, or shorter than those given by the spray programme alone. For our chosen plant-pathogen-fungicide system, the model results suggest that to effectively manage selection for fungicide-resistance, foliar acting systemic seed treatments should be included as one of the maximum number of permitted fungicide applications.

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Systemic Acquired Resistance-Mediated Control of Pine Wilt Disease by Foliar Application With Methyl Salicylate.

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