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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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Induction of PR-1 gene expression Plants of the indicated genotype were inoculated with 1 × 106 bacteria mL-1 DC3000 carrying the specified avirulence gene or the empty vector or a 10 mM MgCl2 blank. At the indicated time points, leaf samples were taken for total RNA preparation. Probes derived from the PR-1 cDNA were used for Northern blots. Quantitation was with a phosphorimager. All blots were stripped and probed again with a radiolabeled probe made from the ROC1 cDNA as a control for RNA loading. These values were used for data normalization. Each bar represents a mean of data from 3 separate experiments. Differences between means were assessed for statistical significance using Student's t tests. Lowercase letters indicate statistically significant differences between means (P < 0.05 or in many cases greater significance). Comparisons of means were made separately for the two time points.
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Figure 2: Induction of PR-1 gene expression Plants of the indicated genotype were inoculated with 1 × 106 bacteria mL-1 DC3000 carrying the specified avirulence gene or the empty vector or a 10 mM MgCl2 blank. At the indicated time points, leaf samples were taken for total RNA preparation. Probes derived from the PR-1 cDNA were used for Northern blots. Quantitation was with a phosphorimager. All blots were stripped and probed again with a radiolabeled probe made from the ROC1 cDNA as a control for RNA loading. These values were used for data normalization. Each bar represents a mean of data from 3 separate experiments. Differences between means were assessed for statistical significance using Student's t tests. Lowercase letters indicate statistically significant differences between means (P < 0.05 or in many cases greater significance). Comparisons of means were made separately for the two time points.

Mentions: The double mutant, each single mutant and Columbia wild-type plants were infected with 1 × 106 bacteria mL-1. At this level of inoculum, most leaf cells did not undergo PCD (data not shown). Macroscopic tissue collapse was therefore not seen, allowing PR-1 gene expression to be quantitated using Northern blots. The data is presented in Figure 2. Columbia wild-type Arabidopsis showed high levels of PR-1 induction in response to either DC3000•avrB or DC3000•avrRpt2. The level of PR-1 induction shown by either single mutant line in response to either bacterial strain was greatly reduced relative to that shown by Columbia. However, both single mutants still showed PR-1 induction at the two day time point in response to either bacterial strain. The level of PR-1 induction shown by the double mutant in response to DC3000•avrRpt2 was not significantly different from that shown in response to either DC3000•empty vector or the MgCl2 blank (Student's t test, P > 0.05). In this experiment, when there was no PCD and NPR1 activity was blocked by mutation, no induction of PR-1 resulted. By contrast, DC3000•avrB did elicit highly significant PR-1 induction (Student's t test, P < 0.01 for comparison to DC3000•empty vector or blank). As NPR1 activity was blocked by mutation, PCD-associated signals likely explain the residual PR-1 induction. These results confirm the original model that the two pathways for PR-1 induction are additive.


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)

Induction of PR-1 gene expression Plants of the indicated genotype were inoculated with 1 × 106 bacteria mL-1 DC3000 carrying the specified avirulence gene or the empty vector or a 10 mM MgCl2 blank. At the indicated time points, leaf samples were taken for total RNA preparation. Probes derived from the PR-1 cDNA were used for Northern blots. Quantitation was with a phosphorimager. All blots were stripped and probed again with a radiolabeled probe made from the ROC1 cDNA as a control for RNA loading. These values were used for data normalization. Each bar represents a mean of data from 3 separate experiments. Differences between means were assessed for statistical significance using Student's t tests. Lowercase letters indicate statistically significant differences between means (P < 0.05 or in many cases greater significance). Comparisons of means were made separately for the two time points.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 2: Induction of PR-1 gene expression Plants of the indicated genotype were inoculated with 1 × 106 bacteria mL-1 DC3000 carrying the specified avirulence gene or the empty vector or a 10 mM MgCl2 blank. At the indicated time points, leaf samples were taken for total RNA preparation. Probes derived from the PR-1 cDNA were used for Northern blots. Quantitation was with a phosphorimager. All blots were stripped and probed again with a radiolabeled probe made from the ROC1 cDNA as a control for RNA loading. These values were used for data normalization. Each bar represents a mean of data from 3 separate experiments. Differences between means were assessed for statistical significance using Student's t tests. Lowercase letters indicate statistically significant differences between means (P < 0.05 or in many cases greater significance). Comparisons of means were made separately for the two time points.
Mentions: The double mutant, each single mutant and Columbia wild-type plants were infected with 1 × 106 bacteria mL-1. At this level of inoculum, most leaf cells did not undergo PCD (data not shown). Macroscopic tissue collapse was therefore not seen, allowing PR-1 gene expression to be quantitated using Northern blots. The data is presented in Figure 2. Columbia wild-type Arabidopsis showed high levels of PR-1 induction in response to either DC3000•avrB or DC3000•avrRpt2. The level of PR-1 induction shown by either single mutant line in response to either bacterial strain was greatly reduced relative to that shown by Columbia. However, both single mutants still showed PR-1 induction at the two day time point in response to either bacterial strain. The level of PR-1 induction shown by the double mutant in response to DC3000•avrRpt2 was not significantly different from that shown in response to either DC3000•empty vector or the MgCl2 blank (Student's t test, P > 0.05). In this experiment, when there was no PCD and NPR1 activity was blocked by mutation, no induction of PR-1 resulted. By contrast, DC3000•avrB did elicit highly significant PR-1 induction (Student's t test, P < 0.01 for comparison to DC3000•empty vector or blank). As NPR1 activity was blocked by mutation, PCD-associated signals likely explain the residual PR-1 induction. These results confirm the original model that the two pathways for PR-1 induction are additive.

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