Introduction

The host–parasite interface formed during infection of plants by biotrophic powdery mildew fungi is a specialised structure involved in the transfer of host nutrients to the fungus (Manners & Gay, 1983; Manners, 1989) and the efficiency with which such pathogens do this makes them highly damaging to crops (Singh et al., 1982). The haustorium is the structure by which the fungus absorbs nutrients from its host. It forms within the epidermal cells, enclosed by an invagination of the host plasma membrane termed the extrahaustorial membrane (ehm); this is separated from the haustorium by the polysaccharide-rich extrahaustorial matrix. All these components collectively make up the haustorial complex (HC; see Fig. 1.).

Powdery mildew fungi are obligate pathogens and exhibit a high degree of host species and cultivar specificity. In certain incompatible combinations of host and pathogen genotype, haustoria are produced but appear to be functionally inactive and so fail to produce elongating secondary hyphae or secondary haustoria (e.g. Erysiphe pisi (Singh & Singh, 1983; Manners & Gay, 1983; Manners, 1989); Erysiphe betae (Dickey & Levy, 1979)). Work on the E. pisi/Pisum sativum system using various cytochemical reagents such as fluorescent lectins, as well as protein and Ca2+-specific fluorochromes has shown that there may be molecular differences between the ehm of haustoria from resistant compared with susceptible interactions (Chard & Gay, 1984). It is therefore a possibility that the molecular recognition events, mediated by the primary products of host genes for resistance and pathogen genes for avirulence (Callow, 1984, 1987) and which are regarded as the first step in resistance triggering through intracellular signalling, are located at this interface.