Assumptions and implications of current gene‐for‐gene hypotheses

Abstract

Molecular biology is helping plant pathologists to achieve some of the principal objectives set in previous decades. Avirulence genes and/or gene products are being isolated (Knogge et al., 1991; Ackerveken et at., 1992; Dangl et al., 1992), and matching resistance genes are being mapped precisely in several plants including peas and Arabidopsis (Debener et al., 1991; Dangl et al., 1992; Fillingham et al., 1992). A gene for resistance to Pseudomonas syringae pv. tomato has been cloned and sequenced (Martin et al., 1993), and more cloned genes have been reported recently at conferences. Typically these contain a leucine-rich repeat motif common to many proteins which are thought to be involved in numerous protein-protein interactions, and a putative ATP/GTP binding site motif (P-loop). Nonetheless, we are still a long way from a comprehensive understanding of all the processes involved in the relationship between host and pathogen, especially those involvmg the highly specialized obligately biotrophic pathogens such as the rusts and powdery mildews of cereals. This is particularly clear from the continuing debate as to whether the specificity of pathogenicity is based on recognition or non-recognition of the pathogen by the host (Heath, 1991; Vanderplank, 1991; Johnson & Knott, 1992). Different types of pathogen, such as facultative and biotrophic types, probably have very different ways of exploiting their hosts and will therefore expose different molecules to their respective host plants during pathogenesis. Thus pathogen recognition in different diseases may be based on recognition genes for different molecules, and responses to different pathogens will then vary depending upon their mode of pathogenicity. The resistance mechanisms available, for example phytoalexin accumulation or cell wall alterations, are thought to be broadly similar in different plants. Two different views of the mechanism of pathogen recognition are commonly held. In simplistic terms, these can be defined as whether pathogens possess the gene products necessary to induce a susceptible response, or whether these gene products induce resistance. In other words, is virulence or avirulence gene expression the active response? The assumptions on which these views are based make them difficult to reconcile and cause confusion in the interpretation of the basic theories developed to explain host-parasite interactions. In this paper we review some of the evidence that should clarify the situation, and we examine some of the implications which follow.