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Title:   Author  item
                                            DE FREITAS, SERGIO - University Of Californiaitem
                                            Jiang, Cai-Zhongitem
                                            MITCHAM, ELIZABETH - University Of California
  Submitted to: Journal of Plant Growth Regulation
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 8/10/2011
                                    Publication  Date: 9/10/2011
                                    Citation: De Freitas, S.T., Jiang, C., Mitcham, E.J. 2011. Mechanisms involved in calcium deficiency development in tomato fruit in response to gibberellins. Journal of Plant Growth Regulation. DOI 10.1007/s00344-011-9233-9.Interpretive Summary: The mechanisms responsible for calcium (Ca) deficiency development in fruit are among the most complex and challenging processes in plants. In tomato fruit, blossom-end rot (BER), considered to be a Ca deficiency disorder, has been studied for more than one hundred years and the mechanisms that trigger this disorder are still not well understood. 
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 varieties ‘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 GA4+7, 300 mg L-1 prohexadione-calcium (Apogee®, GA biosynthesis inhibitor), or water beginning one day after flower pollination. GA4+7 treatment induced an increase in BER incidence in both cultivars up to 100 %, while ‘Ace 55 (Vf)’ and ‘AB2’ plants treated with prohexadione-calcium did not show BER incidence. The number of functional xylem vessels was higher in the placental and pericarp tissue of tomato fruit treated with prohexadione-calcium at early stages of fruit growth. Treatment with prohexadione-calcium also increased pericarp fruit Ca concentration. GA4+7 treatment enhanced the expression of the putative organellar CAX and Ca-ATPase, including CAX3, Ca-ATPase3, and Ca-ATPase5 in both tomato varieties. The lowest water soluble apoplastic Ca concentration and the highest membrane leakage values were observed in pericarp of GA4+7 treated fruit. These results suggest that GAs reduce fruit Ca uptake and water soluble apoplastic Ca concentration, leading to leakier plasma membranes and BER symptom development in fruit tissue.
                                Technical Abstract: Although gibberellins (GAs) have been shown to induce the calcium deficiency disorder, blossom-end rot (BER), development in tomato fruit (Solanum lycopersicum), the mechanisms involved remain largely unexplored. 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 varieties ‘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 GA4+7, 300 mg L-1 prohexadione-calcium (Apogee®, GA biosynthesis inhibitor), or water beginning one day after flower pollination. GA4+7 treatment induced an increase in BER incidence in both cultivars up to 100 %, while ‘Ace 55 (Vf)’ and ‘AB2’ plants treated with prohexadione-calcium did not show BER incidence. The number of functional xylem vessels was higher in the placental and pericarp tissue of tomato fruit treated with prohexadione-calcium at early stages of fruit growth. Treatment with prohexadione-calcium also increased pericarp fruit Ca concentration. GA4+7 treatment enhanced the expression of the putative organellar CAX and Ca-ATPase, including CAX3, Ca-ATPase3, and Ca-ATPase5 in both tomato varieties. The lowest water soluble apoplastic Ca concentration and the highest membrane leakage values were observed in pericarp of GA4+7 treated fruit. These results suggest that GAs reduce fruit Ca uptake and water soluble apoplastic Ca concentration, leading to leakier plasma membranes and BER symptom development in fruit tissue.


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