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. 1998 Dec 8;95(25):15107-11.
doi: 10.1073/pnas.95.25.15107.

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

B P Thomma  1 , K Eggermont, I A Penninckx, B Mauch-Mani, R Vogelsang, B P Cammue, W F Broekaert
Affiliations

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

B P Thomma et al. Proc Natl Acad Sci U S A. .

Abstract

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 pathogen-inducible 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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Figures

Figure 1
Figure 1
Induction of pathogenesis-related genes in Arabidopsis in response to infection with A. brassicicola or to hormone treatment. Four-week-old soil-grown wild-type (Col-0), NahG, npr1–1, and coi1–1 plants were infected with A. brassicicola and harvested 48 hr after treatment. RNA blots were hybridized with the probes indicated on the left of the figure. Symbols above the lanes are as follows: −, mock-inoculated with water; +, inoculated with A. brassicicola spore suspension; 1°, treated lower rosette leaves; 2°, untreated upper rosette leaves. In addition, four-week-old soil-grown wild-type (Col-0) plants were treated with water, 5 mM SA, 0.1% ethanol, or 50 μM MeJA in 0.1% ethanol (MeJA). Plants were harvested 48 hr after treatment, and RNA blots were hybridized with the probes indicated on the left.
Figure 2
Figure 2
Disease development in Arabidopsis inoculated with different fungal pathogens. (A) Four-week-old Arabidopsis plants inoculated with A. brassicicola. Pictures show lesion formation 6 days after inoculation. A typical example of each genotype is shown. (B) Four-week-old Arabidopsis plants inoculated with B. cinerea. Pictures were made 12 days after inoculation (8 days after inoculation for coi1–1). (C) Four-week-old Arabidopsis plants inoculated with P. parasitica strain Wela. Plants were stained with lactophenol-trypan blue (32). Microscopy pictures show blue-stained fungal structures and damaged plant cells in a leaf from plants 11 days after inoculation. A representative example of each genotype is shown. Genotypes are indicated above the pictures.
Figure 3
Figure 3
Quantification of disease development in Arabidopsis inoculated with different fungal pathogens. (A) Average diameter of lesions formed 6 days after inoculation with A. brassicicola. Data represent averages with SDs from measurements of 60 lesions. (B) Percentage fungal RNA of total RNA in infection sites at different times after inoculation of leaves with A. brassicicola. Data points represent measurements on 30 leaf discs. ○, wild-type (Col-0) plants; ⋄, NahG plants; □, npr1–1 plants; ■, coi1–1 plants. (C) Decay of Arabidopsis plants inoculated with B. cinerea. The percentage of dead plants is expressed as a function of time after inoculation. Plants were considered dead when their hearts were completely rotten. Data represent averages with sSDs of four independent experiments performed with 20 plants per genotype. Symbols are as for B.
Figure 4
Figure 4
Protective effect of exogenously applied MeJA and INA after infection by A. brassicicola and P. parasitica. (A) Arabidopsis mutant pad3 was infected with A. brassicicola. Fourty-eight hr before inoculation, separate sets of plants were treated as follows: sprayed with water on the leaves, H2O; sprayed with 1 mg/ml INA wettable powder with 25% active ingredient, INA; untreated in an airtight translucent container, Air; or treated with 150 nM gaseous MeJA in an airtight translucent container, MeJA. Observations were made 6 days after inoculation. (B) Arabidopsis mutant (pad3) and wild-type (Col-0) were infected with P. parasitica strain Noco. Treatments were as described for A. Six days after inoculation, plants were stained with lactophenol-trypan blue (32). Representative microscopy pictures of leaves are shown. Oospores can be seen on plants pretreated with water, air, and MeJA. Plants treated with INA only show signs of local hypersensitive reaction.
Figure 5
Figure 5
Quantification of the protective effect of exogenously applied MeJA and INA on infection by A. brassicicola. (A) Average lesion diameter with SDs from measurements of 30 lesions on pad3 mutants subjected to the indicated pretreatments, as in the legend to Fig. 4A. Experiments were performed three times with similar results. (B) Average lesion diameter with SDs from measurements of 30 lesions on coi1–1 mutants subjected to the indicated pretreatments. Experiments were performed twice with similar results.
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