Induced Systemic Resistance — An Overview

Abstract

It is difficult to understand why it has taken so long for the scientific community and agrichemical industry to recognize the hazards to human health and the environment of the increased dependence on pesticides and to acknowledge the potential of induced systemic resistance in plants and appreciate its significance to fundamental science and as a technology for plant disease control. The early reviews by Chester (Chester, 1933) brought together many descriptions of the phenomenon. This was followed by the well documented experiments by Ross and his colleagues (Ross, 1966), primarily with N-gene tobacco and tobacco mosaic virus, and by reports from my group with green bean, pear, apple, potato, cucumber, muskmelon, watermelon and tobacco and a broad spectrum of pathogens including fungi, bacteria and viruses (Kuć, 1982, 1985, 1987, 1993). What became clear from these reports was that susceptible plants had the genetic information for effective disease resistance mechanisms and that these mechanisms could be expressed systemically for extended periods of time by prior restricted inoculation with pathogens, avirulent forms of pathogens, cultivar-nonpathogenic races, microbial components and chemicals which themselves were not antimicrobial (Kuć, 1982, 1985, 1987, 1991–1993). The reports eroded the concept that a gene for resistance caused the production of a compound which directly inhibited development of a pathogen and susceptible plants, lacking such a gene, could not produce the compound. It was evident that defense compounds were common to resistant and induced resistant plants as well as susceptible plants. This does not preclude mechanisms for resistance in noninduced resistant plants which may be in addition to those induced by biotic or abiotic agents.