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. 1984 Jun;75(2):329–335. doi: 10.1104/pp.75.2.329

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

Ya'Acov Y Leshem 1,2, Sampath Sridhara 1, John E Thompson 1
PMCID: PMC1066906  PMID: 16663620

Abstract

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 (O2τ). 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 O2τ 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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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