Department of Plant Sciences, University of California, Davis, CA 95616, USA.
Plant J. 2012 Sep;71(5):824-35. doi: 10.1111/j.1365-313X.2012.05034.x. Epub 2012 Jun 28.
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.
番茄果实的花端腐烂（BER）被认为是一种钙（Ca²⁺）缺乏症，但对其发病机制知之甚少。我们的假设是，高表达的果胶甲酯酶（PMEs）增加了与细胞壁结合的 Ca²⁺，随后降低了其他细胞功能所需的 Ca²⁺，从而增加了果实对 BER 的易感性。本研究的目的是评估 PME 表达水平、酯化果胶的含量以及与细胞壁结合的 Ca²⁺对番茄果实 BER 发育的影响。野生型和 PME 沉默型番茄植株在温室中生长。在完全开花期，授粉后不再向植物提供 Ca²⁺以诱导 BER。我们的结果表明，在番茄果实中抑制 PMEs 的表达减少了与细胞壁结合的 Ca²⁺的量，同时也降低了果实对 BER 的易感性。野生型和 PME 沉默型果实都具有相似的总组织、胞质和液泡 Ca²⁺浓度，但野生型果实具有较低的水可溶性质外体 Ca²⁺含量和较高的膜泄漏率，这是 BER 的最早症状之一。我们的结果表明，质外体水可溶性 Ca²⁺浓度影响果实对 Ca²⁺缺乏症的易感性。
