Claviceps purpurea is a ubiquitous pathogen of cereals and grasses, causing Ergot disease, which results in substitution of grains by sclerotia. These overwintering structures contain ergot-alkaloids, which can cause severe intoxication in mammals. C. purpurea is an interesting model system for the study of host–pathogen interaction. It displays strict organ specificity, attacking exclusively young grass ovaries. It is optimally adapted to this special niche of infection, probably by mimicry of pollen tubes: there are no resistance genes known, and no effective resistance reactions can be detected in the early steps of infection. In this early phase of host tissue colonization the fungus shows directed, almost unbranched growth towards the base of the ovary. Thus, C. purpurea represents one of the few systems in which directed growth in filamentous fungi can be studied. Finally, the fungus behaves as a true biotroph in planta, although it can be easily grown in axenic culture. We describe here the tools available to study this interesting pathogen, report on recent molecular investigations concerning the role of cell-wall-degrading enzymes and of reactive oxygen species in this specialized interaction, and present an update of the signalling cascades involved in early events of pathogenesis.