Abstract

Phaseollin and pisatin accumulated in bean and pea cotyledons respectively, after incubation at 25 °C following treatment with mercuric chloride. Both the duration of treatment and concentration of mercuric chloride determined maximal phytoalexin concentrations. Highest levels of both phytoalexins occurred when cell damage caused by mercuric chloride was microscopically visible. With increasing amounts of dead cells the concentrations of phytoalexins decreased, and in some treatments no phytoalexins were formed even when some tissue was still alive. The accumulation of phaseollin appeared to be more closely associated with cell death than the accumulation of pisatin. Treatment of cotyledons with mercuric chloride under optimal conditions for phytoalexin formation (10 −3 m for 30 min) led to a loss of electrolytes during the initial 12 h, and to the continuous accumulation of phytoalexins over 5 days. Exudates from mercuric chloride treated cotyledons of both species stimulated phytoalexin accumulation in cut cotyledon bioassays. These results are discussed in relation to current views on the mechanism of phytoalexin accumulation.

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