The hypersensitive response (HR) of plants resistant to microbial pathogens involves a complex form of programmed cell death (PCD) that differs from developmental PCD in its consistent association with the induction of local and systemic defence responses. Hypersensitive cell death is commonl y controlled by direct or indirect interactions between pathogen avirulence gene products and those of plant resistance genes and it can be the result of multiple signalling pathways. Ion fluxes and the generation of reactive oxygen species commonly precede cell death, but a direct involvement of the latter seems to vary with the plant-pathogen combination. Protein synthesis, an intact actin cytoskeleton and salicylic acid also seem necessary for cell death induction. Cytologic al studies suggest that the actual mode and sequence of dismantling the cell contents varies among plant-parasite systems although there may be a universal involvement of cysteine proteases, It seems likely that cell death within the HR acts more as a signal to the rest of the plant rather than as a direct defence mechanism.

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Fungal plant pathogens that attempt to penetrate and feed on living cells frequently trigger a localized plant defence response that results in fungal penetration failure. In the current study we demonstrate that breakdown products of the cell wall released by the localized application of hemicellulase elicit localized responses including, sequentially, extracellular H2O2 generation; accumulation of phenolic compounds; and cross-linking of proteins in the cell wall. In a detailed time-course study of three plant-fungus interactions that result in a high frequency of penetration failure, only one plant-fungus combination displayed a similar profile of responses to that induced by localized cell-wall degradation. The additional generation of extracellular O2- in one interaction, and the absence of phenolic compounds in the cell wall in another, demonstrate that plant responses to the penetration process may be influenced by activities of the penetrating fungus. Significantly, H2O2 generation was the only response detected in all three plant-fungal combinations at the correct time and place to account for penetration failure, and in all three combinations the enzymatic removal of H2O2 resulted in increased penetration success. Pharmacological studies suggest that in two of the three interactions, H2O2 generation required cytoskeletal involvement but was independent of transcription or translation, although inhibition of the latter processes increased fungal penetration. In at least one of these two interactions, the data suggest that H2O2 generation and new gene expression act within the same penetration-inhibiting pathway, possibly through the involvement of phenolic materials. However, enzymatic removal of H2O2 from the third interaction almost completely eliminated penetration failure, while interference with cytoplasmic processes had no effect, suggesting that H2O2 generation in this system did not require protoplast involvement and, alone, was necessary and sufficient to account for fungal penetration failure.

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The transcriptional response of hybrid poplar (Populus trichocarpa x P. deltoides) to poplar leaf rust (Melampsora medusae) infection was studied using the Populus 15.5K cDNA microarray. Pronounced changes in the transcriptome were observed, with approximately 20% of genes on the array showing either induction or repression of transcription within the 9-day infection timecourse. A small number of pathogen-defense genes encoding PR-1, chitinases, and other pathogenesis-related proteins were consistently upregulated throughout the experimental period, but most genes were affected only at individual timepoints. The largest number of changes in gene expression was observed late in the infection at 6 to 9 days postinoculation (dpi). At these timepoints, genes encoding enzymes required for proanthocyanidin (condensed tannin) synthesis were upregulated dramatically. Phytochemical analysis confirmed that, late in the infection, proanthocyanidin levels increased in infected leaves. Strongly M. medusae-repressed genes at 9 dpi included previously characterized wound- and herbivore-induced defense genes, which suggests antagonism between the tree responses to insect feeding and M. medusae infection. In this highly compatible plant-pathogen interaction, we postulate that the biotrophic pathogen evades detection and suppresses early host responses.