Mechanisms Involved in Calcium Deficiency Development in Tomato Fruit in Response to Gibberellins

Although gibberellins (GAs) have been shown to induce development of the physiological disorder blossom-end rot (BER) in tomato fruit (Solanum lycopersicum), the mechanisms involved remain largely unexplored. BER is believed to result from calcium (Ca) deficiency, but the relationship between Ca content and BER incidence is not strong. Our objectives were to better understand how GAs and a GA biosynthesis inhibitor affect BER development in tomato fruit. Tomato plants of two BER-susceptible cultivars, 'Ace 55 (Vf)' and 'AB2,' were grown in a greenhouse environment and subjected to Ca-deficiency conditions. Plants were treated weekly during fruit growth and development with 300 mg L-1 GA(4+7), 300 mg L-1 prohexadione-calcium (Apogee(A (R)), a GA biosynthesis inhibitor), or water beginning 1 day after flower pollination. GA(4+7) treatment induced an increase in BER incidence in both cultivars up to 100%, whereas 'Ace 55 (Vf)' and 'AB2' plants treated with Apogee did not show BER incidence. The number of functional xylem vessels was higher in the placental and pericarp tissue of tomato fruit treated with Apogee at the early stages of fruit growth. Treatment with Apogee also increased fruit pericarp Ca concentration. GA(4+7) treatment enhanced the expression of the putative CAX and Ca-ATPase genes, that code for proteins involved in Ca movement into storage organelles. The lowest water-soluble apoplastic Ca concentration and the highest membrane leakage values were observed in the pericarp of GA(4+7)-treated fruit. These results suggest that GAs consistently reduced fruit Ca uptake and water-soluble apoplastic Ca concentration, leading to leakier plasma membranes and an increase in BER development in fruit tissue of both tomato cultivars.