The quantitative effect of seed production triggers the end of flowering in tomato.

Flowering plants adjust their reproductive period to ensure reproductive success. This involves a tight control of both flower initiation and the termination of the flowering period to optimize resource allocation for seed production. The end of flowering is marked by the cessation of flower production by the inflorescence meristems, which enter a dormant-like state known as proliferative arrest. This process has been mainly studied in Arabidopsis (Arabidopsis thaliana) at the physiological, genetic, and molecular levels but remains to be characterized in other species, which could provide general mechanisms and the groundwork for designing biotechnological strategies aimed at controlling the duration of fruit/seed production. Solanum lycopersicum (tomato) is an excellent model for this goal because of its economic importance and the marked differences in plant architecture, meristem organization, and fruit development. By comparing plants producing fertile and parthenocarpic seedless fruits, we have determined that proliferative arrest in tomato is a reversible process triggered by seed formation. We have identified the seeds as the likely source of signals that instruct the meristems to arrest in a coordinated and quantitative manner. The presence of auxin and abscisic acid in exudates from fertile but not from parthenocarpic fruits and the effect of treating seedless fruits with exogenous auxin on proliferative arrest support a major role of these phytohormones in the communication between seeds and meristems. Our work supports the conservation of factors controlling proliferative arrest in flowering plants while providing insights into the regulation of this process.