Abstract

Here we focused on tip-burn and blossom-end rot (BER) symptoms in the tomato plants expressing the constitutively active form of Ca 2+ /H + antiporter (sCAX1) and/or a Ca-binding protein (calreticulin, CRT) genes during their whole growth period. Conclusively we demonstrated that CRT is able to suppress the tip-burn and BER symptoms that were induced by sCAX1. Under poor nutrition con- dition, tomato plants overexpressing sCAX1 showed severe necrotic collapses in both roots and shoot polar tissues, which are in accordance with Ca 2+ deficient symptoms frequently observed in an agricultural cultivation of tomato. Reciprocal grafting trials using sCAX1 and wild type plants revealed that the tip-burn symptom by sCAX1 overexpression is not caused by hindrance of Ca 2+ uptake from soil. We con- structed CRT overexpressing transgenic tomatoes, and crossed them with sCAX1 transgenic plants to investigate the effects of CRT on the symptoms of sCAX1 transgenic plants. Co- expression of sCAX1 and CRT significantly suppressed the Ca 2+ deficient symptoms of sCAX1 transgenic plants. Those results suggest the model that Ca 2+ homeostasis disturbed by the overexpression of sCAX1 may be suppressed by the co-expression of CRT.

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