Superoxide Generation in Chemically Activated Resistance of Barley in Response to Inoculation with the Powdery Mildew Fungus

Abstract

AbstractIn a previous work, a phenotype‐specific accumulation of superoxide radical anions (O•−2) after attack of the powdery mildew fungus (Blumeria [syn. Erysiphe] graminis f.sp. hordei) in near‐isogenic barley (Hordeum vulgare L.) lines bearing different Mlx genes for resistance was described (Hückelhoven and Kogel, 1998). We have now a histochemical study of the pathogenesis‐related O•−2 generation in the systemic activated resistance (SAR) response induced in barley cv Pallas by the plant activator 2,6‐dichloroisonicotinic acid (DCINA).SAR‐specific defence was conducted prevalently characterized by penetration resistance. Fungal arrest was observed before haustorium formation by a highly localized cell wall reinforcement (effective papillae) and, in most cases, by a subsequent hypersensitive cell death (HR). No O•−2 generation was found in association with these plant defence responses. However, a strong O•−2 burst in the attacked epidermal cells was detected in the control plants which were not activated by DCINA. This burst coincided with cell wall penetration and subsequent contact of the pathogen with the host plasma membrane.A strong SAR‐related O•−2 burst was induced in the mesophyll tissue beneath the attacked and hypersensitively reacting epidermal cells in plants treated with DCINA. The accumulation of O•−2 was confined to chloroplasts. The remarkable burst in mesophyll tissue was not followed by mesophyll‐HR indicating that chloroplastic O•−2 generation is not sufficient for the hypersensitive cell death. Since the same pattern of pathogenesis‐related O•−2 accumulation was identified for race‐specific response mediated by the Mlg gene for powdery mildew resistance, the present data are consistent with the hypothesis that the SAR phenotype is a phenocopy of the Mlg‐type resistance (Kogel et al., 1994).