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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-5 gene expression Experimental procedures and data analysis were done the same way as with PR-1 gene expression experiments (Figure 2).
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Figure 3: Induction of PR-5 gene expression Experimental procedures and data analysis were done the same way as with PR-1 gene expression experiments (Figure 2).

Mentions: The two postulated pathways acting in an additive fashion sufficed to explain bacterial induction of SAR and PR-1 gene expression. Experiments were next undertaken to extend the model to the control of PR-5 induction. DC3000•avrRpt2 or DC3000•avrB were inoculated into ndr1-1/npr1-2 double mutant plants, the single mutants, or the Columbia wild type plants. PR-5 gene expression was quantitated by Northern blots. The data is presented in Figure 3. At the one day time point, the double mutant showed significant impairment in PR-5 induction relative to wild type in response to either avirulent bacterial strain (Student's t test, P < 0.05). However, at the two day time point, only the impairment in response to DC3000•avrRpt2 was statistically significant at this level. If the criteria for statistically significant differences was relaxed to P < 0.1, then the same qualitative picture was shown as with PR-1 in comparison of single mutants to wild type Columbia. Columbia plants showed differences at this level of significance from ndr1-1 or npr1-2 plants in induction of PR-5 in response to DC3000•avrRpt2 at both time points. These results are consistent with contributions to PR-5 induction coming from both the HR-associated pathway and the SA/NPR1-dependent pathway. However, PR-5 gene expression occurred in spite of blockade of both pathways in experiments with DC3000•avrRpt2 and the double mutant. This result was very different from what was seen with PR-1 induction or SAR. Clearly, the two pathways we have delineated do not constitute a complete picture of signaling leading to PR-5 gene expression.


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-5 gene expression Experimental procedures and data analysis were done the same way as with PR-1 gene expression experiments (Figure 2).
© Copyright Policy
Related In: Results  -  Collection

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

Figure 3: Induction of PR-5 gene expression Experimental procedures and data analysis were done the same way as with PR-1 gene expression experiments (Figure 2).
Mentions: The two postulated pathways acting in an additive fashion sufficed to explain bacterial induction of SAR and PR-1 gene expression. Experiments were next undertaken to extend the model to the control of PR-5 induction. DC3000•avrRpt2 or DC3000•avrB were inoculated into ndr1-1/npr1-2 double mutant plants, the single mutants, or the Columbia wild type plants. PR-5 gene expression was quantitated by Northern blots. The data is presented in Figure 3. At the one day time point, the double mutant showed significant impairment in PR-5 induction relative to wild type in response to either avirulent bacterial strain (Student's t test, P < 0.05). However, at the two day time point, only the impairment in response to DC3000•avrRpt2 was statistically significant at this level. If the criteria for statistically significant differences was relaxed to P < 0.1, then the same qualitative picture was shown as with PR-1 in comparison of single mutants to wild type Columbia. Columbia plants showed differences at this level of significance from ndr1-1 or npr1-2 plants in induction of PR-5 in response to DC3000•avrRpt2 at both time points. These results are consistent with contributions to PR-5 induction coming from both the HR-associated pathway and the SA/NPR1-dependent pathway. However, PR-5 gene expression occurred in spite of blockade of both pathways in experiments with DC3000•avrRpt2 and the double mutant. This result was very different from what was seen with PR-1 induction or SAR. Clearly, the two pathways we have delineated do not constitute a complete picture of signaling leading to PR-5 gene expression.

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