Abstract

Cultured parsley (Petroselinum crispum) cells or protoplasts respond to treatment with a crude cell wall preparation from the soybean pathogen Phytophthora megasperma f.sp. glycinea (Pmg elicitor) with the transcriptional activation of the same set of defense-related genes as are activated in parsley leaves upon infection with fungal spores [1-4]. In contrast, local necrosis and callose apposition which were found to be early plant responses to fungal infection [5] were not stimulated in cultured cells by elicitor treatment. Proteinaceous components of the Pmg elicitor were identified as the elicitor-active substances [6]. A 42-kDa glycoprotein elicitor was purified from fungal culture filtrate [7] that was also present in hyphal cell walls of the fungus grown in planta [8]. Its heat-stabile elicitor activity was found to reside exclusively in the protein moiety [7]. While the elicitor activity was destroyed by digestion with trypsin or pronase E, it was almost completely retained after treatment with endoprotease Glu-C [9]. The fragments released from the 42-kDa glycoprotein by endoprotease Glu-C were separated by reverse-phase HPLC, individually tested for elicitor activity and sequenced by automated Edman degradation [10]. An oligopeptide consisting of 13 amino acids with the sequence, H2N-VWNQPVRGFKVYE-COOH (Pep-13) and several larger fragments that all contained Pep-13 were found to induce phytoalexin synthesis in parsley protoplasts. Pep-13 itself stimulated the same responses as the Pmg elicitor, namely defense gene activation, formation of phytoalexins, an oxidative burst, Ca2+ and H+ influx as well as an efflux of K+ and Cl-ions [10].KeywordsElicitor ActivityCell Wall PreparationAutomate Edman DegradationPetroselinum CrispumFungal Culture FiltrateThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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