The Association of “Pathogenesis‐related” Proteins with Viral Induced Necrosis in Nicotiana sylvestris

Abstract

AbstractThe association of “pathogenesis‐related” (PR) proteins with protection from superinfection, systemic acquired resistance and production of localized necrotic lesions was examined with a system using tobacco mosaic virus (TMV) and Nicotiana sylvestris. Leaves of N. sylvestris with a mosaic from earlier inoculation with a systemically infecting strain of TMV (TMV‐C) and control plants were challenged with a necrotizing strain of TMV (TMV‐P), RNA of TMV‐P and turnip mosaic virus (TuMV). TMV‐P virions produced localized necrotic lesions only in the dark green areas of the mosaic of TMV‐C infected plants. Both RNA of TMV‐P and TuMV produced localized necrotic lesions in both light green and dark green areas of the mosaic of TMV‐C infected plants. All three challenge inocula produced localized necrotic lesions in previously uninoculated plants. Six days after challenge inoculation proteins were extracted from separated dark green and light green mosaic leaf tissue, and leaf material from control plants. Proteins were separated by electrophoresis in a 5 % polyacrylamide spacer gel and 10 % polyacrylamide running gel. PR proteins were found in tissue where localized necrotic lesions were produced as a result of challenge inoculation, but not in tissue that was not superinfected. PR proteins were not found in light green or dark green mosaic leaf tissue as a result of TMV‐C inoculation. No PR proteins were evident in protein extracts from light green tissue challenged with TMV‐P, although PR proteins were produced in dark green tissue, where necrosis occurred, from the same leaves. Systemic acquired resistance (reduction in size of lesions formed by a challenge inoculation) to TuMV or RNA of TMV‐P and PR protein concentration was measured at various times in light green areas of mosaic leaves where dark green areas of the mosaic leaves had been inoculated with TMV‐P. No quantitative or temporal relationship between the onset of resistance and PR protein production was found. It is concluded that PR proteins are a result of pathogen induced necrosis and not significantly involved in the mechanism(s) of viral induced resistance.