Partners and International Organizations
(English)
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C. Castresana (E), P. Rodriguez-Palenzuela (E), M. Daniels (UK), K. van Loon (NL), R. Linders (NL)
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Abstract
(English)
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Plants inoculated with necrotizing pathogens can express resistance against the same or different pathogens in parts of the plant physically distinct from the first inoculation. This has been termed systemic acquired resistance (SAR). Induction of SAR is dependent on salicylic acid, Mutants of Arabidopsis thaliana have confirmed the involvement of a salicylic acid -dependent pathway in SAR. A second type of induced resistance, termed induced systemic resistance (ISR) was found to be induced in leaves by root colonizing fluorescent Pseudomonads. Unlike SAR, ISR is dependent on ethylene and jasmonate. During ISR, pathogenesis-related proteins (PRs) are not induced but, interestingly, it was shown that SAR and ISR pathways are not totally independent. For instance, Arabidopsis mutants defective in the NPR1 (non inducer of PR1) protein show neither induction of SAR nor ISR.
In this project, the presence of yet another signal transduction pathway leading to resistance was demonstrated. We have demonstrated that b-aminobutyric acid (BABA) has a surprising action independent of the known signals involved in induced resistance. Our objective was to study the mode of action of BABA in the protection of Arabidopis plants against pathogens. We found that BABA protected Arabidopsis against the oomycete pathogen Peronospora parasitica or Botrytis cinerea through activation of natural defense mechanisms of the plant such as callose deposition, the hypersensitive response (HR), and the formation of trailing necroses. BABA was still fully protective against P. parasitica in transgenic plants or mutants impaired in the salicylic acid, jasmonic acid and ethylene signaling pathways. Against Botrytis, BABA was also active in jasmonic acid and ethylene-insensitive mutants but was inactive inactive in plants impaired in the SAR pathway. Treatment with BABA did not induce the accumulation of mRNA of the systemic acquired resistance-associated PR-1 and the ethylene- and jasmonic acid-dependent PDF1.2 genes. However, BABA potentiated the accumulation of PR-1 mRNA after attack by virulent pathogenic bacteria. As a result, BABA-treated Arabidopsis plants were less diseased compared to the untreated control. In the case of bacteria, BABA protected mutants insensitive to jasmonic acid and ethylene, but was not active in plants impaired in the SAR transduction pathway. Thus, BABA protects Arabidopsis against different virulent pathogens by potentiating pathogen-specific plant resistance mechanisms. In addition, we have provided evidence that BABA-mediated papilla formation after P. parasitica infection is independent of the classical SAR signaling pathway. Mutants insensitive to the action of BABA were also isolated and are now available to investigate the proteins involved in the mode of action of BABA.
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