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.