Mycorrhiza‐induced resistance in citrus against Tetranychus urticae is plant‐species dependent and inversely correlated to basal immunity
María Manresa‐Grao, Victoria Pastor, Paloma Sánchez‐Bel, Ana Cruz, Miguel Cerezo, Josep A. Jaques, Víctor Flors- Insect Science
- Agronomy and Crop Science
- General Medicine
Abstract
BACKGROUND
Mycorrhizal plants show enhanced resistance to biotic stresses, but few studies address mycorrhiza‐induced resistance (MIR) against biotic challenges in woody plants and particularly in citrus. Here we present a comparative study of two citrus species, Citrus aurantium, which is resistant, and Citrus reshni, which is highly susceptible to Tetranychus urticae. Although both mycorrhizal species are protected in locally infested leaves, they show very distinct responses to MIR.
RESULTS
Previous studies indicated that C. aurantium is insensitive to MIR in systemic tissues and MIR‐triggered antixenosis. Conversely, C. reshni is highly responsive to MIR which triggers local, systemic and indirect defence, and antixenosis against the pest. Transcriptional, hormonal, and inhibition assays in C. reshni indicated regulation of JA‐ and ABA‐dependent responses in MIR. The phytohormone JA‐Ile and JA acid biosynthesis gene LOX2 are primed at early time‐points. Evidence indicates a metabolic flux from phenylpropanoids to specific flavones that are primed at 24 h post infestation (hpi). MIR also triggers priming of naringenin in mycorrhizal C. reshni, which shows a strong correlation with several flavones and JA‐Ile that overaccumulate in mycorrhizal plants. Treatments with an inhibitor of phenylpropanoid biosynthesis C4H enzyme impaired resistance and reduced the symbiosis, demonstrating that phenylpropanoids and derivatives mediate MIR in C. reshni.
CONCLUSION
Altogether, MIR effectiveness is inversely correlated to basal immunity in different citrus species, and it provides multifaceted protection in the susceptible C. reshni against T. urticae activating rapidly local, and systemic defenses that are mainly regulated by the accumulation of specific flavones and priming of JA‐dependent responses.
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