Resistance gene-dependent plant defense responses.

Abstract

Plants are constantly being challenged by aspiring pathogens, but disease is rare. Why? Broadly, there are three reasons for pathogen failure. Either (1) the plant is unable to support the niche requirements of a potential pathogen and is thus a non? host; or (2) the plant possesses preformed structural barriers or toxic compounds that confine successful infections to specialized pathogen species; or (3) upon recognition of the attacking pathogen, defense mechanisms are elaborated and the invasion remains localized. All three types of interaction are said to be incompatible, but only the latter resistance mech? anism depends on induced responses. Successful pathogen invasion and disease (compatibility) ensue if the preformed plant defenses are inappropriate, the plant does not detect the pathogen, or the activated defense responses are ineffective. In this review, we examine the essential prerequisites for patho? gen recognition and the induction of localized defense responses. Preformed defenses are considered elsewhere in this issue (see Osbourn, 1996, in this issue). Race-specific pathogen recognition is hypothesized to re? sult from the direct or indirect interaction of the product of a dominant or semidominant plant resistance (R) gene with a product derived from the corresponding dominant pathogen avirulence (Avr) gene (Keen, 1992; Staskawicz et al., 1995). Subsequent signal transduction events are assumed to coordinate the activation of an array of defense responses. This simple model appears to explain much but begs many questions. For example, R gene products are likely to provide key components for recognition, but how do the distinct classes of R proteins characterized to date (see Bent, 1996, in this is? sue) activate the defense response? Do different R gene classes activate distinct responses? The regulation of some components of defense mechanisms has been studied in plant cell cultures in response to non-race-specific elicitors, but to what extent do such studies provide a model for R gene func? tion? Plant resistance is often correlated with the activation of specific defense responses, but which (if any) are required to abolish or retard pathogen growth, and how? Which are pri? mary responses and which are secondary? Does the first response involve transcriptional regulation, the activation of preformed enzymes, and/or the opening of ion channels, or