Auxin and Gibberellin Interact in Citrus Fruit Set
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AuthorBermejo, Almudena; Granero, Beatriz; Mesejo, Carlos; Reig, Carmina; Tejedo, Vicente; Agustí, Manuel; Primo-Millo, Eduardo; Iglesias, Domingo J.
Cita bibliográficaBermejo, A., Granero, B., Mesejo, C., Reig, C., Tejedo, V., Agustí, M., Primo-Millo, E., Iglesias, D. J. (2017). Auxin and gibberellin interact in citrus fruit set. Journal of Plant Growth Regulation, 37, 491-500.
Gibberellins (GA) and auxin (indole-3-acetic acid, IAA) are considered the main compounds involved in the induction of fruit set. Citrus trees flower profusely but exhibit dramatically low fruit set rates and, in particular, seeded orange cultivars also require pollination for fruit to adequately set. Consequently, they represent an excellent model to investigate the interactions between both hormones and their effect on fruit set and development. Unpollinated ovaries from ‘Pineapple’ sweet orange trees were treated with IAA and pollinated ones with TIBA (2,3,5-triiodobenzoic acid, inhibitor of auxin transport), and changes in ovaries were registered shortly after the treatments. The highest IAA levels were found in unpollinated ovaries treated with auxin (twofold increase compared to pollinated ones), and the lowest corresponded to pollinated ones supplemented with TIBA (30% reduction). GA content also differed substantially among samples. In general, expression of the GA-biosynthetic gene GA20ox2 in the ovule and pericarp paralleled the changes in GA20 content in both tissues, and also expression of GA3ox1 and GA1 content but only in the ovule. The levels of these GA in unpollinated ovaries were promoted in response to exogenous IAA, whereas expression of the GA-inactivation gene GA2ox1 and the concentration of the GA-catabolite GA8 were reduced by this treatment. Significantly, treatments with GA3 or IAA to unpollinated ovaries recovered fruit set to the level reached by free pollinated ones. Our study demonstrates that IAA alters GA metabolism in citrus leading to marked changes in the active GA1 levels in ovules and pericarp, mainly through the regulation of GA-biosynthetic genes and the inhibition of the catabolic pathway.