Role of Pectin Methylesterases On Cellular Ca2+ Distribution and Blossom-End Rot Development in Tomato Fruit.

Although blossom-end rot (BER) is believed to be a Ca²⁺ deficiency disorder, there is limited information about the mechanisms involved in its development in tomato fruit. Blossom-end rot has been associated with increased membrane leakage and low apoplastic Ca²⁺ concentrations. Our objective was to evaluate the effect of pectin methyl esterase (PME) expression on Ca²⁺ binding to the cell wall and BER development in tomato fruit. Wild type and PME silenced tomato plants were grown in a greenhouse environment in 9.5 L pots containing 0.3 kg of perlite as substrate. The plants were irrigated everyday with a nutrient solution containing all essential nutrients. At full bloom, flowers were manually pollinated and Ca²⁺ was no longer fed to the plants to induce BER development. Blossom-end rot incidence was higher in wild type fruit than in PME silenced fruit at 30 and 45 days after pollination (DAP). PME silenced fruit pericarp showed lower membrane leakage and higher water soluble apoplastic Ca²⁺ content than wild type fruit at 30 and 45 DAP. PME silenced fruit had lower expression of PMEs. In situ immunolocalization analysis shows higher accumulation of deesterified pectins close to the plasma membrane in wild type fruit pericarp cells. The degree of water soluble and insoluble pectin esterification was lower in wild type fruit at 30 and 45 DAP. Total tissue Ca²⁺ concentration was similar in wild type and PME silenced fruit. Water soluble pectin had higher Ca²⁺ concentration in wild type fruit at 45 DAP. Calcium concentration in water insoluble pectin fraction and fruit firmness were higher in wild type fruit at 30 and 45 DAP. The results indicate that high PME expression decreases pectin esterification, which increases Ca²⁺ bound to the cell wall, decreasing water soluble apoplastic Ca²⁺, and increasing membrane leakage, which leads to BER development in tomato fruit under low Ca²⁺ conditions.