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We have examined the characteristics of cell death induced by pathogen infection in oats with respect to following hallmark apoptotic features: DNA laddering, chromatin condensation, and electron microscopic-terminal deoxynucleotidyl transferase-mediated UTP end labeling positive response. A wide range of plant pathogens representing different levels of parasitism in susceptible and resistant interactions were used for the inocula, which include (i) an obligate parasite, Puccinia coronata f. sp. avenae (the crown rust fungus); (ii) a facultative biotroph parasite, Magnaporthe grisea (the blast fungus); (iii) pathogenic bacteria, Pseudomonas syringae pv. atropurpurea and P syringae pv. coronafaciens (the halo or stripe blights of oats); and (iv) Ryegrass mottle virus. Surprisingly, any of the pathogens used induced most of the apoptotic features in oat cells at and around the infection sites, indicating that apoptotic cell death is a common phenomenon in oats during pathogen attack. The localization and the timing of apoptotic cell death during a course of infection were, however, quite different depending on the interactions (compatible or incompatible) and the pathogens (fungi, bacteria, or viruses). Possible roles of apoptotic cell death in the susceptible and resistant interactions are discussed.
The activation of plant defense mechanisms upon pathogen infection is often accompanied by cell death, termed hypersensitive response (HR), at and around the infection sites. HR is a typical reaction of a resistant plant against an incompatible pathogen, where rapid and localized cell death occurs and the pathogen invasion is halted (Heath 2000). This response is invoked by infection with a wide range of pathogenic organisms, including fungi, bacteria, viruses, and nematodes (Morel and Dangl 1997). Recent studies have suggested that hypersensitive cell death is a genetically programmed response and shares a number of morphological and biochemical features with animal apoptosis (Dangl et al. 1996; Gilchrist 1998; Heath 1998; Lam et al. 2001; Ponder et al. 1998; Richberg et al. 1998; Tada et al. 2001). For example, cell death triggered in resistant cowpea plants by an incompatible cowpea rust fungus (Uromyces vignae) was accompanied by DNA laddering and a terminal deoxynucleotidyl transferase-mediated UTP end labeling (TUNEL)-positive response (Ryerson and Heath 1996). Also, caspase-like proteolytic activity (del Pozo and Lam 1998) and Ca^sup 2+^-dependent nucleases were detected in resistant tobacco plants during the process of HR upon infection...