Abstract

Based on results from previously published work, various chemical solutions were injected into the intercellular spaces of uninfected bean plant leaves in an attempt to induce or prevent (after subsequent infection with Uromyces vignae) the plant cell wall autofluorescence or increased wall refractivity normally induced by unsuccessful fungal infection. Solutions included pectinase, cellulysin, protease, driselase, digitonin, CaCl 2, the Ca 2+ ionophore A23187, Gramicidin A, weak acids, bases and buffers, fusicoccin, vanadate, H 2O 2, paraquat, ferulate, reduced glutathione, the ethylene inhibitor aminoethoxyvinyl glycine, the ethylene precursor aminocyclopropane-1-curboxylic acid, and the ethylene analogue 2-chloroethylphosphonic acid (ethephon). None of the injected solutions proved capable of eliciting the reactions and of the more limited variety of solutions tested in infected tissues, only ethephon and superoxide dismutase reduced the incidence of these responses in infected leaves. Ethephon induced susceptibility to U. vignae, allowing an increased number of haustoria to be formed in infected bean plants. Exudates from the pathogen Uromyces appendiculatus or the non-pathogen U. vignae did not elicit these responses either. These data suggest that the elicitation of wall autofluorescence and increased wall refractivity in leaves of intact Phaseolus vulgaris plants does not involve processes suggested as important in the elicitation of other plant defense responses.

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