Abstract
Different types of stress, such as hypersensitive reaction to viruses or necrotic response induced by chemical and mechanical injuries, caused similar patterns in early electrolyte leakage from discs of cowpea leaves. The electrolyte leakage, suggestive of permeability alterations, always occurred in advance of cell death. Altered permeability can therefore be considered as an aspecific response to stress and a marker of necrogenesis. No correlation was found between permeability alterations and the mechanism for virus localization, the main characteristic of the hypersensitive reaction, because tobacco rattle virus induced similar alterations in either incompatible cowpea or compatible tobacco plants. Early Ca2+ losses occurred following viral and abiotic necrogenic stresses. The external supply of Ca2+ to cowpea during the course of the hypersensitivity to viruses failed to effect pathogenesis, assessed as the number and size of the resulting necrotic local lesions, and the release of electrolyte leakage from the infected leaves. However, the external supply of Ca2+ counteracted the negative effect of EDTA, a chelating agent, on the resistance of cowpea leaves to cell-to-cell spread of viruses, suggesting that a Ca2+-deficiency may weaken the mechanism of defense of the cells against the localized viral infection.