Pathogenesis-related proteins and systemic resistance to blue mould and tobacco mosaic virus induced by tobacco mosaic virus, Peronospora tabacina and aspirin

Abstract

Stem injection with sporangiospores of Peronospora tabacina or inoculation of leaves with tobacco mosaic virus (TMV) induced systemic protection in tobacco against blue mould and disease caused by the virus. Protection against blue mould induced by TMV was first detected 3 days after inoculation with TMV, reached a maximum after 12 days, and persisted for at least 26 days. Removal of the TMV-infected leaves at intervals after inoculation with TMV resulted in a similar time course for protection. Leaves which expanded after induction with TMV were better protected against blue mould than leaves which were expanded before induction. Protection of such plants against TMV, however, was uniform throughout the plant. Spraying leaves with 0.05 % acetylsalicylic acid (ASA) protected only the treated leaves against blue mould and TMV, whereas repeated stem injection of ASA induced systemic protection against TMV but not blue mould. SDS-PAGE of pathogenesis-related (PR) proteins extracted from TMV or P. tabacina induction sites and protected uninfected leaves of induced plants indicated that the appearance of PR proteins coincided with the appearance of protection. Systemic protection against TMV induced by stem injection with ASA, however, was not associated with PR proteins. The PR proteins appeared at higher levels but were qualitatively similar in leaves which expanded after induction with TMV as compared to leaves which were expanded at the time of induction. After challenge with P. tabacina, PR proteins accumulated earlier and to higher levels in plants induced with P. tabacina or TMV than in controls. Some of the PR proteins were detected in intercellular fluids of induced plants before challenge. The pattern of PR proteins appeared qualitatively identical following induction with P. tabacina and TMV. The induction of systemic protection and PR proteins does not appear to be due to a unique component of the inducing pathogen but rather is the result of a common metabolic perturbation caused by the pathogens.