The phytoalexins kievitone and phaseollin were quantified in hypocotyls of Phaseolus vulgaris infected by either Rhizoctonia solani or fusarium solani f.sp. phaseoli. Infection of intact seedlings produced a pattern of phytoalexin accumulation consistent with earlier reports. In response to R. solani, kievitone accumulated rapidly and may have been instrumental in .the formation of restricted lesions; little kievitone could be detected in hypocotyls bearing spreading lesions produced by f. solani f.sp. phaseoli.

These results prompted the development of an artificial inoculation system employing excised, cored hypocotyls to investigate the possibility that the observed disparity in kievitone levels might reflect differential production, by the two fungi, of (an) elicitor(s) of kievitone accumulation. While this system did not exactly reproduce the response of intact plants upon inoculation with mycelium, it did provide a sensitive means for the evaluation of kievitone-eliciting activity in culture filtrates and mycelial fractions.

Material capable of eliciting high levels of kievitone in the artificial system was isolated from cell-free mycelial extracts of ft. solani; the same procedures failed to demonstrate similar activity in f. solani f.sp. phaseoli. Kievitone-eliciting activity was also solubilized from cell walls of R. solani. Since the active fractions were only partially-purified, a thorough appraisal of the structure and activity of the elicitor(s) was not achieved.

An elicitor preparation from R. solani, introduced into bean hypocotyls prior to inoculation with F. solani f.sp. phaseoli, appeared to delay colonization by this aggressive fungus. This finding raises the possibility of cross-protecting plants through the action of phytoalexins.

Hypotheses to explain the observed differences in the resistance of bean hypocotyls to the two fungi are outlined in the context of current ideas on the elicitation of phytoalexin accumulation and disease resistance.