Involvement of Calcium and Calmodulin in Membrane Deterioration during Senescence of Pea Foliage

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Abstract
The prospect that Ca2+ promotes senescence by activating calmodulin was examined using cut pea (P. sativum cv. Alaska) foliage as a model system. Senescence was induced by severing 17-day old plants from their roots and maintaining them in aqueous test solutions in the dark for an additional 4 days. Treatment of the foliage with the Ca2+ ionophore (A23187) during the senescence-induction period promoted a lateral phase separation of the bulk lipids in microsomal membranes, indicating that internalization of Ca2+ facilitates membrane deterioration. In addition, microsomal membranes from ionophore-treated tissue displayed an increased capacity to convert 1-aminocyclopropane-1-carboxylic acid to ethylene and an increased propensity to produce the superoxide anion .**GRAPHIC**. Treatment of the tissue with fluphenazine during the senescence-induction period, which prevents binding of the Ca:calmodulin complex to enzymes, delayed membrane deterioration as measured by these criteria. It also proved possible to simulate these in situ effects of the Ca2+ ionophore on ethylene production and .**GRAPHIC**. formation by treating microsomal membranes isolated from young tissue with phospholipase A2 in the presence of Ca2+ and calmodulin; these effects of phospholipase A2 and Ca:calmodulin were inhibited by calmodulin antagonists. The observations collectively suggest that internalized Ca2+ promotes senescence by activating calmodulin, which in turn mediates the action of phospholipase A2 on membranes.