Accumulation of salicylic acid and PR-1 gene transcripts in relation to the systemic acquired resistance (SAR) response induced by Pseudomonas syringae pv. tomato in Arabidopsis

• Published in: Physiological and molecular plant pathology 1999-08, Vol.55 (2), p.121-130
• Main Authors: CAMERON, ROBIN K., PAIVA, NANCY L., LAMB, CHRIS J., DIXON, RICHARD A.
• Format: Article
• Language: English
• Subjects: alleles; Arabidopsis; Arabidopsis thaliana; Bacterial plant pathogens; Biological and medical sciences; chemical constituents of plants; defense mechanisms; experimental infections; Fundamental and applied biological sciences. Psychology; gene expression; hypersensitive response; induced resistance; messenger RNA; mutants; pathogenesis-related proteins; Pathology. Damages, economic importance; Phytopathology. Animal pests. Plant and forest protection; PR-1; Pseudomonas syringae pv. tomato; Pseudomonas syringae pv. tomato , Arabidopsis thaliana; Pseudomonas syringae tomato; rps2-101C; rps2-201; salicylic acid; systemic acquired resistance; virulence
• ISSN: 0885-5765; 1096-1178
• DOI: 10.1006/pmpp.1999.0214

The relationship between salicylic acid (SA) accumulation, PR-1 gene expression, and the degree of systemic acquired resistance (SAR) established in Arabidopsis plants has been determined by comparing the response of wild-type ecotype Columbia (Col-0) and two hypersensitive response (HR)-defective mutants (rps2-201 andrps2-101C ) during the SAR response induced by avirulent Pseudomonas syringae pv. tomato (Pst). Unlike wild-type Col-0 plants, plants harboring either mutant allele were unable to manifest a SAR response. During the initiation/immunization stage of SAR, PR-1 gene expression was delayed in interactions which did not lead to SAR (avirulent inoculation of rps2-201 and rps2-101C, or inoculation with virulent bacteria in wild-type Col-0) compared to those interactions that did lead to SAR (avirulent inoculation of wild-type Col-0). PR-1 expression was reduced in the rps mutants compared to wild-type plants during the establishment and manifestation stage and therefore correlated with the ability to elicit a SAR response. SA accumulated to similar levels during the establishment and manifestation stages for Col-0 and therps2 mutant alleles. Therefore the ability to accumulate SA was not predictive of the ability to elicit SAR, and SA accumulation alone is not sufficient to elicit the SAR response. Moreover, SA accumulated to similar levels during both compatible (virulent infections) and incompatible interactions (avirulent infections). However, SA accumulation was reduced in the initiation/immunization stage of SAR in rps2-101C compared to wild-type, but not in rps2-201 , suggesting that this reduction was related to an HR-specific defect mediated by the rps2-101C mutant allele.