Ph.D. student University of Tsukuba Tsukuba, Ibaraki, Japan
Body of Abstract: The production of tomato (Solanum lycopersicum), a model plant for fleshy fruit development, depends on the efficiency of fruit set, the transition of ovary into fruit. Pollination is normally required for fruit set but it is negatively impacted by adverse conditions such as high temperature. Parthenocarpy, the pollination-independent fruit set, is an attractive trait for horticultural crops, although the detailed molecular mechanism remains elusive. We isolated the novel parthenocarpic mutant, Sldad1 (Solanum lycopersicum defective in anther dehiscence1), from ‘Micro-Tom’ EMS mutagenesis library. The causative gene, SlDAD1, encodes an Arabidopsis DAD1 homologous gene which is involved in jasmonate (JA) biosynthesis. However, how JA regulates fruit set is poorly understood.
SlDAD1 transcript was exclusively observed in the filament before flowering, and JA content was correlated with its transcript level in the filament. However, JA also accumulated in the ovary before flowering. Using imaging techniques, JA was predominantly accumulated in the filament and ovary, especially in the ovule. These results suggested that JA synthesized in the filament before flowering is transported and accumulated in the ovule, suppressing tomato fruit set. The morphology of Sldad1 ovule was abnormal around embryo sac at anthesis, although anther structure and pollen germination ratio were comparable between WT and Sldad1 mutant. Among the genes expressed in ovules, ethylene (ET)-related gene was upregulated in the WT ovaries before flowering. Additionally, ET precursor 1-aminocyclopropane-1-carboxylic acid (ACC) production of Sldad1 ovaries was significantly reduced compared with that of WT at anthesis. Indeed, the gene knockout showed parthenocarpy. Here, we propose a hypothesis that JA in the ovule partially suppresses tomato fruit set through ET.