The 2011 ASHS Annual Conference

There has been more than one hundred years of research on Ca deficiency disorders in fruit, but the mechanisms involved remain poorly understood. Studies have shown a positive correlation between low tissue Ca and high fruit susceptibility to Ca deficiency disorders. However, there is no predictive accuracy between Ca content and Ca deficiency symptom development in fruit. New evidence suggests that Ca deficiency development should not be studied only at the whole tissue level, but also at the cellular level, where reduction in specific pools of Ca may lead to a cellular localized Ca deficiency and cell death. Our studies revealed that fruit with adequate or high total tissue Ca will not develop Ca deficiency symptoms with proper regulation of cellular Ca partitioning and distribution. However, the same fruit will develop Ca deficiency symptoms if abnormal regulation of cellular Ca partitioning and distribution occurs, leading to a depletion of specific cellular pools of Ca, cellular localized Ca deficiency and finally cell death. In addition, low fruit Ca uptake may cause a reduction in all cellular pools of Ca, resulting in fruit that are more susceptible to Ca deficiency development. In our studies, spraying tomato plants weekly with 500 mg L^-1 ABA prevented BER development by reducing xylemic water and Ca movement into the leaves and increasing it into the fruit. The increase in fruit Ca uptake was possibly favored by an increase in the number of functional xylem vessels in the fruit, as well as a reduction in the phloem/xylem ratio of fruit sap uptake. In another study, tomato fruit expressing a constitutively functional Arabidopsis thaliana Ca²⁺/H⁺ exchanger (sCAX1), a tonoplast protein that pumps Ca into the vacuole, showed a steady increase in BER development until 100% incidence 15 days after pollination. Wild type fruit did not develop any BER. Further analysis showed that sCAX1-expressing fruit pericarp had two-fold higher total Ca content, lower apoplastic and cytosolic Ca contents, and higher Ca accumulation in the vacuole of sCAX1-expressing cells, compared to wild type fruit tissue. We also showed that decreasing pectin methylesterase expression in tomato fruit reduces binding sites for Ca in the cell wall, which increases other pools of Ca in the cell, eventually reducing fruit susceptibility to BER. Our results support the hypothesis that fruit susceptibility to Ca deficiency disorders is determined not only by fruit Ca uptake, but also by mechanisms controlling cellular Ca partitioning and distribution.