Role of pectin methylesterases in cellular calcium distribution and blossom-end rot development in tomato fruit
Article first published online: 28 JUN 2012
© 2012 The Authors. The Plant Journal © 2012 Blackwell Publishing Ltd
The Plant Journal
Volume 71, Issue 5, pages 824–835, September 2012
How to Cite
de Freitas, S. T., Handa, A. K., Wu, Q., Park, S. and Mitcham, E. J. (2012), Role of pectin methylesterases in cellular calcium distribution and blossom-end rot development in tomato fruit. The Plant Journal, 71: 824–835. doi: 10.1111/j.1365-313X.2012.05034.x
- Issue published online: 24 AUG 2012
- Article first published online: 28 JUN 2012
- Accepted manuscript online: 8 MAY 2012 01:21AM EST
- Received 8 February 2011; revised 19 April 2012; accepted 23 April 2012; Published online 28 June 2012.
- cell wall;
- calcium deficiency;
Blossom-end rot (BER) in tomato fruit (Solanum lycopersicum) is believed to be a calcium (Ca2+) deficiency disorder, but the mechanisms involved in its development are poorly understood. Our hypothesis is that high expression of pectin methylesterases (PMEs) increases Ca2+ bound to the cell wall, subsequently decreasing Ca2+ available for other cellular functions and thereby increasing fruit susceptibility to BER. The objectives of this study were to evaluate the effect of PME expression, and amount of esterified pectins and Ca2+ bound to the cell wall on BER development in tomato fruit. Wild-type and PME-silenced tomato plants were grown in a greenhouse. At full bloom, flowers were pollinated and Ca2+ was no longer provided to the plants to induce BER. Our results show that suppressing expression of PMEs in tomato fruit reduced the amount of Ca2+ bound to the cell wall, and also reduced fruit susceptibility to BER. Both the wild-type and PME-silenced fruit had similar total tissue, cytosolic and vacuolar Ca2+ concentrations, but wild-type fruit had lower water-soluble apoplastic Ca2+ content and higher membrane leakage, one of the first symptoms of BER. Our results suggest that apoplastic water-soluble Ca2+ concentration influences fruit susceptibility to Ca2+ deficiency disorders.