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Articles

Involvement of Calcium and Calmodulin in Membrane Deterioration during Senescence of Pea Foliage ¹

Department of Biology, University of Waterloo, Waterloo, Ontario N2L 3G1, Canada

The prospect that Ca²⁺ promotes senescence by activating calmodulin has been examined using cut pea (Pisum sativum co 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 (O₂). 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 O₂ formation by treating microsomal membranes isolated from young tissue with phospholipase A₂ in the presence of Ca²⁺ and calmodulin, and 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.

¹ Supported by the Natural Sciences and Engineering Research Council of Canada.

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