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Two pathways act in an additive rather than obligatorily synergistic fashion to induce systemic acquired resistance and PR gene expression.

Zhang C, Shapiro AD - BMC Plant Biol. (2002)

Bottom Line: Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, PR-1 and PR-5.One of these pathways is NPR1-independent and depends on signals associated with hypersensitive cell death.At least two other pathways also contribute additively to PR-5 induction.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Plant and Soil Sciences, Delaware Agricultural Experiment Station, College of Agriculture and Natural Resources, University of Delaware, Newark, DE, USA. zhangchu@udel.edu

ABSTRACT

Background: Local infection with necrotizing pathogens induces whole plant immunity to secondary challenge. Pathogenesis-related genes are induced in parallel with this systemic acquired resistance response and thought to be co-regulated. The hypothesis of co-regulation has been challenged by induction of Arabidopsis PR-1 but not systemic acquired resistance in npr1 mutant plants responding to Pseudomonas syringae carrying the avirulence gene avrRpt2. However, experiments with ndr1 mutant plants have revealed major differences between avirulence genes. The ndr1-1 mutation prevents hypersensitive cell death, systemic acquired resistance and PR-1 induction elicited by bacteria carrying avrRpt2. This mutation does not prevent these responses to bacteria carrying avrB.

Results: Systemic acquired resistance, PR-1 induction and PR-5 induction were assessed in comparisons of npr1-2 and ndr1-1 mutant plants, double mutant plants, and wild-type plants. Systemic acquired resistance was displayed by all four plant lines in response to Pseudomonas syringae bacteria carrying avrB. PR-1 induction was partially impaired by either single mutation in response to either bacterial strain, but only fully impaired in the double mutant in response to avrRpt2. PR-5 induction was not fully impaired in any of the mutants in response to either avirulence gene.

Conclusion: Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, PR-1 and PR-5. One of these pathways is NPR1-independent and depends on signals associated with hypersensitive cell death. The other pathway is dependent on salicylic acid accumulation and acts through NPR1. At least two other pathways also contribute additively to PR-5 induction.

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DC3000•avrB elicits systemic acquired resistance on the ndr1-1/npr1-2 double mutant and both single mutants Plants were either inoculated with 2 × 107 bacteria mL-1 DC3000•avrB (white bars) or not inoculated (black bars). Two days later, inoculated leaves were excised. Remaining leaves were pressure infiltrated using a syringe with 5 × 104 bacteria mL-1 DC3000•empty vector. Data points represent means of triplicate (Day 0) or quintuplicate (Day 2 or 4) determinations of in planta bacterial growth.
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Figure 1: DC3000•avrB elicits systemic acquired resistance on the ndr1-1/npr1-2 double mutant and both single mutants Plants were either inoculated with 2 × 107 bacteria mL-1 DC3000•avrB (white bars) or not inoculated (black bars). Two days later, inoculated leaves were excised. Remaining leaves were pressure infiltrated using a syringe with 5 × 104 bacteria mL-1 DC3000•empty vector. Data points represent means of triplicate (Day 0) or quintuplicate (Day 2 or 4) determinations of in planta bacterial growth.

Mentions: If NPR1 is truly essential for SAR [9], npr1 mutant plants should not be able to undergo SAR in response to P. syringae pv. tomato DC3000 (hereafter DC3000) carrying avrB. Alternatively, if HR-associated signals leading to SAR act independently of NPR1, DC3000•avrB might be able to elicit SAR on npr1 plants. The results of this experiment are presented in Figure 1. Columbia, wild type plants showed a three order of magnitude reduction in growth of virulent bacteria in plants that had received a prior inoculation with DC3000•avrB. SAR was also displayed by ndr1-1 mutant plants. These results are comparable to those published previously [4]. Clear SAR was also displayed by the npr1-2 mutant. The SAR response was statistically significant (Student's t test, P < 0.05) for all three lines in this experiment and in a replicate experiment. This assay is not sufficiently sensitive to quantitate small differences in SAR between the lines. However, it is clear that all three lines did display SAR. As it is likely that both mutant lines are alleles (previously established for ndr1-1[6] and argued below for npr1-2), the hypothesis that NPR1 is essential for SAR is thus rejected.


Two pathways act in an additive rather than obligatorily synergistic fashion to induce systemic acquired resistance and PR gene expression.

Zhang C, Shapiro AD - BMC Plant Biol. (2002)

DC3000•avrB elicits systemic acquired resistance on the ndr1-1/npr1-2 double mutant and both single mutants Plants were either inoculated with 2 × 107 bacteria mL-1 DC3000•avrB (white bars) or not inoculated (black bars). Two days later, inoculated leaves were excised. Remaining leaves were pressure infiltrated using a syringe with 5 × 104 bacteria mL-1 DC3000•empty vector. Data points represent means of triplicate (Day 0) or quintuplicate (Day 2 or 4) determinations of in planta bacterial growth.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC130961&req=5

Figure 1: DC3000•avrB elicits systemic acquired resistance on the ndr1-1/npr1-2 double mutant and both single mutants Plants were either inoculated with 2 × 107 bacteria mL-1 DC3000•avrB (white bars) or not inoculated (black bars). Two days later, inoculated leaves were excised. Remaining leaves were pressure infiltrated using a syringe with 5 × 104 bacteria mL-1 DC3000•empty vector. Data points represent means of triplicate (Day 0) or quintuplicate (Day 2 or 4) determinations of in planta bacterial growth.
Mentions: If NPR1 is truly essential for SAR [9], npr1 mutant plants should not be able to undergo SAR in response to P. syringae pv. tomato DC3000 (hereafter DC3000) carrying avrB. Alternatively, if HR-associated signals leading to SAR act independently of NPR1, DC3000•avrB might be able to elicit SAR on npr1 plants. The results of this experiment are presented in Figure 1. Columbia, wild type plants showed a three order of magnitude reduction in growth of virulent bacteria in plants that had received a prior inoculation with DC3000•avrB. SAR was also displayed by ndr1-1 mutant plants. These results are comparable to those published previously [4]. Clear SAR was also displayed by the npr1-2 mutant. The SAR response was statistically significant (Student's t test, P < 0.05) for all three lines in this experiment and in a replicate experiment. This assay is not sufficiently sensitive to quantitate small differences in SAR between the lines. However, it is clear that all three lines did display SAR. As it is likely that both mutant lines are alleles (previously established for ndr1-1[6] and argued below for npr1-2), the hypothesis that NPR1 is essential for SAR is thus rejected.

Bottom Line: Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, PR-1 and PR-5.One of these pathways is NPR1-independent and depends on signals associated with hypersensitive cell death.At least two other pathways also contribute additively to PR-5 induction.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Plant and Soil Sciences, Delaware Agricultural Experiment Station, College of Agriculture and Natural Resources, University of Delaware, Newark, DE, USA. zhangchu@udel.edu

ABSTRACT

Background: Local infection with necrotizing pathogens induces whole plant immunity to secondary challenge. Pathogenesis-related genes are induced in parallel with this systemic acquired resistance response and thought to be co-regulated. The hypothesis of co-regulation has been challenged by induction of Arabidopsis PR-1 but not systemic acquired resistance in npr1 mutant plants responding to Pseudomonas syringae carrying the avirulence gene avrRpt2. However, experiments with ndr1 mutant plants have revealed major differences between avirulence genes. The ndr1-1 mutation prevents hypersensitive cell death, systemic acquired resistance and PR-1 induction elicited by bacteria carrying avrRpt2. This mutation does not prevent these responses to bacteria carrying avrB.

Results: Systemic acquired resistance, PR-1 induction and PR-5 induction were assessed in comparisons of npr1-2 and ndr1-1 mutant plants, double mutant plants, and wild-type plants. Systemic acquired resistance was displayed by all four plant lines in response to Pseudomonas syringae bacteria carrying avrB. PR-1 induction was partially impaired by either single mutation in response to either bacterial strain, but only fully impaired in the double mutant in response to avrRpt2. PR-5 induction was not fully impaired in any of the mutants in response to either avirulence gene.

Conclusion: Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, PR-1 and PR-5. One of these pathways is NPR1-independent and depends on signals associated with hypersensitive cell death. The other pathway is dependent on salicylic acid accumulation and acts through NPR1. At least two other pathways also contribute additively to PR-5 induction.

Show MeSH
Related in: MedlinePlus