Find in Library

<p>Abstract</p> <p>Background</p> <p>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 <it>PR-1</it> but not systemic acquired resistance in <it>npr1</it> mutant plants responding to <it>Pseudomonas syringae</it> carrying the avirulence gene <it>avrRpt2</it>. However, experiments with <it>ndr1</it> mutant plants have revealed major differences between avirulence genes. The <it>ndr1-1</it> mutation prevents hypersensitive cell death, systemic acquired resistance and <it>PR-1</it> induction elicited by bacteria carrying <it>avrRpt2</it>. This mutation does not prevent these responses to bacteria carrying <it>avrB</it>.</p> <p>Results</p> <p>Systemic acquired resistance, <it>PR-1</it> induction and <it>PR-5</it> induction were assessed in comparisons of <it>npr1-2</it> and <it>ndr1-1</it> mutant plants, double mutant plants, and wild-type plants. Systemic acquired resistance was displayed by all four plant lines in response to <it>Pseudomonas syringae</it> bacteria carrying <it>avrB</it>. <it>PR-1</it> 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 <it>avrRpt2</it>. <it>PR-5</it> induction was not fully impaired in any of the mutants in response to either avirulence gene.</p> <p>Conclusion</p> <p>Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, <it>PR-1</it> and <it>PR-5</it>. One of these pathways is <it>NPR1</it>-independent and depends on signals associated with hypersensitive cell death. The other pathway is dependent on salicylic acid accumulation and acts through <it>NPR1</it>. At least two other pathways also contribute additively to <it>PR-5</it> induction.</p>