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Ethylene, a gaseous plant hormone, plays a role in plant development, defense, and climacteric fruit ripening. Both genetic and biochemical evidence suggest that the response of plants to ethylene is mediated by a specific ethylene receptor. The signal emanating from the receptor-effector complex is then presumably transduced via an unknown cascade pathway. We have used the plant pathogenesis response, exemplified by the induction of the pathogenesis-related gene chitinase, as a paradigm to investigate ethylene-dependent signal transduction in the plant cell. We showed that calcium is necessarily involved in the ethylene-mediated pathogenesis response. Blocking calcium fluxes with chelators inhibited ethylene-dependent induction of chitinase accumulation, but not ethylene independent induction. Artificially increasing cytosolic calcium levels by treatments with the calcium ionophore ionomycin or the calcium pump blocker thapsigargin stimulated chitinase accumulation. Plants grown in calcium-poor soil showed a 10-fold reduction in leaf extractable calcium. Their leaves exhibited a reduced pathogenesis reaction to ethylene and were impaired in another hormone response mediated by calcium, i.e., abscisic acid-controlled closure of guard cells. The addition of calcium to leaves excised from calcium-deficient plants restored their sensitivity to ethylene. Ethylene participates in the control of seedling growth, promoting the so-called "triple response" that results in distinct morphological development, such as hypocotyl hook formation. This effect, similar to the ethylene-promoted pathogenesis response, was found to be calcium dependent. The results indicate that calcium is required for a variety of ethylene-dependent processes.

Calcium Requirement for Ethylene-Dependent Responses.