Infection of wheat by Septoria tritici was studied in a compatible (cultivar 'Sevin'-isolate IPO323) and an incompatible (cultivar 'Stakado'-isolate IPO323) interaction. A second incompatible interaction (cultivar 'Flame'-isolate IPO323) was included as a control of the most important observations made for Stakado. Quantitative studies of the initial stages of infection confirmed that penetration occurs through stomata. However, direct penetration attempts were also observed, indicated by papilla-formation. Pre-penetration growth and penetration frequency was not different between the interactions. Hyphal growth in Stakado was inhibited after penetration and no pycnidia formed whereas in Sevin, hyphal growth progressed and pycnidia formed 15 days after inoculation. Significantly higher amounts of H(2)O(2) accumulated in Stakado than in Sevin until 11 days after inoculation. Timing and localization of H(2)O(2) in Stakado correlated with arrest of pathogen growth, thus indicating a role for this molecule in resistance. H(2)O(2) accumulation is known to arrest biotrophic pathogens and therefore also likely the hemibiotrophic pathogen S. tritici. More H(2)O(2) accumulated in Sevin than Stakado 13 and 15 days after inoculation, coinciding with pycnidium formation and host cell collapse. This late accumulation in the compatible interaction is thought to be a stress-related response. After inoculation with S. tritici, total peroxidase activity and gene transcript of an apoplastic peroxidase increased in Stakado. The peroxidase activity pattern and transcript accumulation profile suggest a role for peroxidase in resistance, probably in cell wall cross-linking. Accumulation patterns of the gene transcript of a catalase and the total catalase enzyme activity suggest roles for catalase synthesis and inactivation in regulating H(2)O(2) accumulation. (C) 2003 Elsevier Ltd. All rights reserved.