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Pisatin Accumulation and Lesion Development in Peas Infected with Aphanomyces euteiches, Fusarium solani f. sp. pisi, or Rhizoctonia solani. Steven G. Pueppke, Graduate Research Assistant, Plant Pathology Department, Cornell University, Ithaca, N.Y. 14850; Hans D. Van Etten, Assistant Professor, Plant Pathology Department, Cornell University, Ithaca, N.Y. 14850. Phytopathology 64:1433-1440. Accepted for publication 4 June 1974. DOI: 10.1094/Phyto-64-1433.

Pea seedlings were inoculated with the root and/or epicotyl-rotting pathogens Aphanomyces euteiches, Fusarium solani f. sp. pisi or Rhizoctonia solani. At given time intervals after inoculation, lesions were excised, and their volumes and pisatin contents were determined. A. euteiches lesions expanded rapidly for 5 days, although by 36 h after inoculation pisatin concn in infected tissue was eight times greater than that required to completely prevent growth of the pathogen in vitro. Pisatin concn in lesion tissue decreased after 36 h, yet the quantity of pisatin per lesion increased as the lesion enlarged. Although margins of older lesions usually extended beyond the hyphal front, pisatin was almost uniformly distributed throughout colonized and uncolonized tissue. In Rhizoctonia-infected tissue, the amount of pisatin per lesion, pisatin concn in the lesions, and lesion volume increased coincidentally, reaching plateaus 6 days after inoculation. Pisatin concn in 2-day-old Rhizoctonia lesions was considerably greater than quantities which were inhibitory in vitro, yet the lesions continued to expand. In F. solani f. sp. pisi lesions, pisatin concns of up to 5 mg/cm³ were found; however, the pathogen was insensitive to pisatin in vitro. The presence of substantial quantities of pisatin in the young expanding lesions containing the sensitive pathogen A. euteiches has not been reconciled with the concept of pisatin as a disease resistance factor in peas.