Kh. Kogel et R. Huckelhoven, Superoxide generation in chemically activated resistance of barley in response to inoculation with the powdery mildew fungus, J PHYTOPATH, 147(1), 1999, pp. 1-4
Citations number
18
Categorie Soggetti
Plant Sciences
Journal title
JOURNAL OF PHYTOPATHOLOGY-PHYTOPATHOLOGISCHE ZEITSCHRIFT
In 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 Mis genes for resistance was described (Huckelh
oven and Kogel, 1998). We have now a histochemical study of the pathogenesi
s-related O-2(.-) generation in the systemic activated resistance (SAR) res
ponse induced in barley cv Pallas by the plant activator 2,6-dichloroisonic
otinic acid (DCINA).
SAR-specific defence was conducted prevalently characterized by penetration
resistance. Fungal arrest was observed before haustorium formation by a hi
ghly localized cell wall reinforcement (effective papillae) and, in most ca
ses, by a subsequent hypersensitive cell death (HR). No O-2(.-) generation
was found in association with these plant defence responses. However, a str
ong O-2(.-) burst in the attacked epidermal cells was detected in the contr
ol plants which were not activated by DCINA. This burst coincided with cell
wall penetration and subsequent contact of the pathogen with the host plas
ma membrane.
A strong SAR-related O-2(.-) burst was induced in the mesophyll tissue bene
ath the attacked and hypersensitively reacting epidermal cells in plants tr
eated with DCINA. The accumulation of O-2(.-) was confined to chloroplasts
The remarkable burst in mesophyll tissue was not followed by mesophyll-HR i
ndicating that chloroplastic O-2(.-) generation is not sufficient for the h
ypersensitive cell death. Since the same pattern of pathogenesis-related O-
2(.-) accumulation was identified for race-specific response mediated by th
e Mlg gene for powdery mildew resistance, the present data are consistent w
ith the hypothesis that the SAR phenotype is a phenocopy of the Mlg-type re
sistance (Kogel et al., 1994).