Inhibition of auxin transport from the ovary or from the apical shoot induces parthenocarpic fruit-set in tomato mediated by gibberellins.

Fruit-set in tomato (Solanum lycopersicum) depends on gibberellins and auxins (GAs). Here, we show, using the cv MicroTom, that application of N-1-naphthylphthalamic acid (NPA; an inhibitor of auxin transport) to unpollinated ovaries induced parthenocarpic fruit-set, associated with an increase of indole-3-acetic acid (IAA) content, and that this effect was negated by paclobutrazol (an inhibitor of GA biosynthesis). NPA-induced ovaries contained higher content of GA(1) (an active GA) and transcripts of GA biosynthetic genes (SlCPS, SlGA20ox1, and -2). Interestingly, application of NPA to pollinated ovaries prevented their growth, potentially due to supraoptimal IAA accumulation. Plant decapitation and inhibition of auxin transport by NPA from the apical shoot also induced parthenocarpic fruit growth of unpollinated ovaries. Application of IAA to the severed stump negated the plant decapitation effect, indicating that the apical shoot prevents unpollinated ovary growth through IAA transport. Parthenocarpic fruit growth induced by plant decapitation was associated with high levels of GA(1) and was counteracted by paclobutrazol treatment. Plant decapitation also produced changes in transcript levels of genes encoding enzymes of GA biosynthesis (SlCPS and SlGA20ox1) in the ovary, quite similar to those found in NPA-induced fruits. All these results suggest that auxin can have opposing effects on fruit-set, either inducing (when accumulated in the ovary) or repressing (when transported from the apical shoot) that process, and that GAs act as mediators in both cases. The effect of NPA application and decapitation on fruit-set induction was also observed in MicroTom lines bearing introgressed DWARF and SELF-PRUNING wild-type alleles.

Auxin-induced fruit-set in tomato is mediated in part by gibberellins.

Tomato (Solanum lycopersicum L.) fruit-set and growth depend on gibberellins (GAs). Auxins, another kind of hormone, can also induce parthenocarpic fruit growth in tomato, although their possible interaction with GAs is unknown. We showed that fruit development induced by the auxins indole-3-acetic acid and 2,4-dichlorophenoxyacetic acid (2,4-D) were significantly reduced by the simultaneous application of inhibitors of GA biosynthesis, and that this effect was reversed by the application of GA(3). This suggested that the effect of auxin was mediated by GA. Parthenocarpic fruits induced by 2,4-D had higher levels of the active GA(1), its precursors and metabolites, than unpollinated non-treated ovaries, but similar levels as those found in pollinated ovaries. Application experiments of radioactive-labelled GAs to unpollinated ovaries showed than 2,4-D altered GA metabolism (both biosynthesis and catabolism) in vivo. Transcript levels of genes encoding copalyldiphosphate synthase (SlCPS), SlGA20ox1, SlGA20ox2 and SlGA20ox3, and SlGA3ox1 were higher in unpollinated ovaries treated with 2,4-D. In contrast, transcript levels of SlGA2ox2 (out of the five SlGA2ox genes known to encode this kind of GA-inactivating enzyme) were lower in ovaries treated with 2,4-D. Our results support the idea that auxins induce fruit-set and growth in tomato, at least partially, by enhancing GA biosynthesis (GA 20-oxidase, GA 3-oxidase and CPS), and probably by decreasing GA inactivation (GA2ox2) activity, thereby leading to higher levels of GA(1). The expression of diverse Aux/indole-3-acetic acid (IAA) and auxin response factors, which may be involved in this effect of auxin, was also altered in 2,4-D-induced ovaries.

Gibberellin regulation of fruit set and growth in tomato.

The role of gibberellins (GAs) in tomato (Solanum lycopersicum) fruit development was investigated. Two different inhibitors of GA biosynthesis (LAB 198999 and paclobutrazol) decreased fruit growth and fruit set, an effect reversed by GA(3) application. LAB 198999 reduced GA(1) and GA(8) content, but increased that of their precursors GA(53), GA(44), GA(19), and GA(20) in pollinated fruits. This supports the hypothesis that GA(1) is the active GA for tomato fruit growth. Unpollinated ovaries developed parthenocarpically in response to GA(3) > GA(1) = GA(4) > GA(20), but not to GA(19), suggesting that GA 20-oxidase activity was limiting in unpollinated ovaries. This was confirmed by analyzing the effect of pollination on transcript levels of SlCPS, SlGA20ox1, -2, and -3, and SlGA3ox1 and -2, encoding enzymes of GA biosynthesis. Pollination increased transcript content of SlGA20ox1, -2, and -3, and SlCPS, but not of SlGA3ox1 and -2. To investigate whether pollination also altered GA inactivation, full-length cDNA clones of genes encoding enzymes catalyzing GA 2-oxidases (SlGA2ox1, -2, -3, -4, and -5) were isolated and characterized. Transcript levels of these genes did not decrease early after pollination (5-d-old fruits), but transcript content reduction of all of them, mainly of SlGA2ox2, was found later (from 10 d after anthesis). We conclude that pollination mediates fruit set by activating GA biosynthesis mainly through up-regulation of GA20ox. Finally, the phylogenetic reconstruction of the GA2ox family clearly showed the existence of three gene subfamilies, and the phylogenetic position of SlGA2ox1, -2, -3, -4, and -5 was established.