Acquired Resistance in Barley (The Resistance Mechanism Induced by 2,6-Dichloroisonicotinic Acid Is a Phenocopy of a Genetically Based Mechanism Governing Race-Specific Powdery Mildew Resistance)

Kogel, K. H.; Beckhove, Uli; Dreschers, J.; Münch, Steffen; Romme, Y.

doi:10.1104/pp.106.4.1269

Cited by 120 publications

(47 citation statements)

References 33 publications

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“…On the other hand, MeJA failed to protect wheat against the powdery mildew fungus Erysiphe graminis (26), whereas SA-mimicking compounds such as INA and benzothiadiazole conferred effective protection (18,26). We have shown that at least protection of Arabidopsis against A. brassicicola infection is caused by activation of responses that require a functional JA signal-transduction pathway, as the protection was observed for the pad3 mutant but not for the JA-insensitive coi1-1 mutant.…”

Section: Discussionmentioning

confidence: 85%

Separate jasmonate-dependent and salicylate-dependent defense-response pathways in Arabidopsis are essential for resistance to distinct microbial pathogens

Thomma

Eggermont

Penninckx

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

1,347

1,025

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The endogenous plant hormones salicylic acid (SA) and jasmonic acid (JA), whose levels increase on pathogen infection, activate separate sets of genes encoding antimicrobial proteins in Arabidopsis thaliana. The pathogeninducible genes PR-1, PR-2, and PR-5 require SA signaling for activation, whereas the plant defensin gene PDF1.2, along with a PR-3 and PR-4 gene, are induced by pathogens via an SA-independent and JA-dependent pathway. An Arabidopsis mutant, coi1, that is affected in the JA-response pathway shows enhanced susceptibility to infection by the fungal pathogens Alternaria brassicicola and Botrytis cinerea but not to Peronospora parasitica, and vice versa for two Arabidopsis genotypes (npr1 and NahG) with a defect in their SA response. Resistance to P. parasitica was boosted by external application of the SA-mimicking compound 2,6-dichloroisonicotinic acid [Delaney, T., et al. (1994) Science 266, 1247-1250] but not by methyl jasmonate (MeJA), whereas treatment with MeJA but not 2,6-dichloroisonicotinic acid elevated resistance to Alternaria brassicicola. The protective effect of MeJA against A. brassicicola was the result of an endogenous defense response activated in planta and not a direct effect of MeJA on the pathogen, as no protection to A. brassicicola was observed in the coi1 mutant treated with MeJA. These data point to the existence of at least two separate hormone-dependent defense pathways in Arabidopsis that contribute to resistance against distinct microbial pathogens.

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Section: Discussionmentioning

confidence: 85%

Separate jasmonate-dependent and salicylate-dependent defense-response pathways in Arabidopsis are essential for resistance to distinct microbial pathogens

Thomma

Eggermont

Penninckx

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

1,347

1,025

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“…The CIR response to Bgh correlates with enhanced epidermal cell death, papillae formation, and highly localized H 2 O 2 accumulation (24,28). The onset of CIR was accompanied by down-regulation of BI-1, whereas overexpression of BI-1 resulted in induced susceptibility (Figs.…”

Section: Figmentioning

confidence: 99%

Overexpression of barley BAX inhibitor 1 induces breakdown of mlo -mediated penetration resistance to Blumeria graminis

Hückelhoven

Dechert²,

Kögel³

2003

Proc. Natl. Acad. Sci. U.S.A.

175

137

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Cell death regulation is linked to pathogen defense in plants and animals. Execution of apoptosis as one type of programmed cell death in animals is irreversibly triggered by cytochrome c release from mitochondria via pores formed by BAX proteins. This type of programmed cell death can be prevented by expression of BAX inhibitor 1 (BI-1), a membrane protein that protects cells from the effects of BAX by an unknown mechanism. In barley, a homologue of the mammalian BI-1 is expressed in response to inoculation with the barley powdery mildew fungus Blumeria graminis f.sp. hordei (Bgh). We found differential expression of BI-1 in response to Bgh in susceptible and resistant plants. Chemical induction of resistance to Bgh by soil drench treatment with 2,6-dichloroisonicotinic acid led to down-regulation of the expression level of BI-1. Importantly, single-cell transient overexpression of BI-1 in epidermal leaf tissue of susceptible barley cultivar Ingrid led to enhanced accessibility, resulting in a higher penetration efficiency of Bgh on BI-1-transformed cells. In Bgh-resistant mlo5 genotypes, which do not express the negative regulator of defense and cell death MLO, overexpression of BI-1 almost completely reconstituted susceptibility to fungal penetration. We suggest that BI-1 is a regulator of cellular defense in barley sufficient to substitute for MLO function in accessibility to fungal parasites.

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“…(Hijwegen et al, 1996), barley (Hordeum vulgare) (Kogel et al, 1994), and rice (Oryza sativa) (Métraux et al, 1991) from a number of pathogens. Two synthetic compounds structurally related to INA were also reported to induce resistance in rice (Yoshida et al, 1990;Seguchi et al, 1992).…”

mentioning

confidence: 99%

Gene-Expression Patterns and Levels of Jasmonic Acid in Rice Treated with the Resistance Inducer 2,6-Dichloroisonicotinic Acid

1997

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Acquired Resistance in Barley (The Resistance Mechanism Induced by 2,6-Dichloroisonicotinic Acid Is a Phenocopy of a Genetically Based Mechanism Governing Race-Specific Powdery Mildew Resistance)

Cited by 120 publications

References 33 publications

Separate jasmonate-dependent and salicylate-dependent defense-response pathways in Arabidopsis are essential for resistance to distinct microbial pathogens

Separate jasmonate-dependent and salicylate-dependent defense-response pathways in Arabidopsis are essential for resistance to distinct microbial pathogens

Overexpression of barley BAX inhibitor 1 induces breakdown of mlo -mediated penetration resistance to Blumeria graminis

Gene-Expression Patterns and Levels of Jasmonic Acid in Rice Treated with the Resistance Inducer 2,6-Dichloroisonicotinic Acid

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