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Mauch-Mani, Brigitte
Résultat de la recherche
Interplay between JA, SA and ABA signalling during basal and induced resistance against Pseudomonas syringae and Alternaria brassicicola
2007, Flors, Victor, Ton, Jurriaan, van Doorn, Ronald, Jakab, Gabor, GarcÃa-AgustÃn, Pilar, Mauch-Mani, Brigitte
We have examined the role of the callose synthase PMR4 in basal resistance and β-aminobutyric acid-induced resistance (BABA-IR) of Arabidopsis thaliana against the hemi-biotrophic pathogen Pseudomonas syringae and the necrotrophic pathogen Alternaria brassicicola. Compared to wild-type plants, the pmr4-1 mutant displayed enhanced basal resistance against P. syringae, which correlated with constitutive expression of the PR-1 gene. Treating the pmr4-1 mutant with BABA boosted the already elevated levels of PR-1 gene expression, and further increased the level of resistance. Hence, BABA-IR against P. syringae does not require PMR4-derived callose. Conversely, pmr4-1 plants showed enhanced susceptibility to A. brassicicola, and failed to show BABA-IR. Wild-type plants showing BABA-IR against A. brassicicola produced increased levels of JA. The pmr4-1 mutant produced less JA upon A. brassicicola infection than the wild-type. Blocking SA accumulation in pmr4-1 restored basal resistance, but not BABA-IR against A. brassicicola. This suggests that the mutant's enhanced susceptibility to A. brassicicola is caused by SA-mediated suppression of JA, whereas the lack of BABA-IR is caused by its inability to produce callose. A. brassicicola infection suppressed ABA accumulation. Pre-treatment with BABA antagonized this ABA accumulation, and concurrently potentiated expression of the ABA-responsive ABI1 gene. Hence, BABA prevents pathogen-induced suppression of ABA accumulation, and sensitizes the tissue to ABA, causing augmented deposition of PMR4-derived callose.
β-Aminobutyric Acid-induced Resistance in Plants
2001, Jakab, Gabor, Cottier, Valérie, Toquin, Valérie, Rigoli, Ghislaine, Zimmerli, Laurent, Métraux, Jean-Pierre, Mauch-Mani, Brigitte
The broad sprectrum protective effect of the non-protein amino acid β-aminobutyric acid (BABA) against numerous plant diseases has been well-documented in the literature. Here, we present an overview of BABA-induced protection in various pathosystems. Contriidictory reports concerning the mechanism of action underlying this type of protection incited us to take advantage of Arabidopsis/pathogen interactions as model systems to investigate the action of BABA at the genetic and molecular level. We present evidence that the protective effect of BABA is due to a potentiation of natural defense mechanisms against biotic and abiotic stresses. In order to dissect the pathways involved in potentiation by BABA describe the use of a mutational approach based on BABA-induced female sterility in Arabidopsis.