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Interplay between JA, SA and ABA signalling during basal and induced resistance against Pseudomonas syringae and Alternaria brassicicola
Authors:Flors Victor  Ton Jurriaan  van Doorn Ronald  Jakab Gabor  García-Agustín Pilar  Mauch-Mani Brigitte
Institution:Laboratory of Molecular and Cellular Biology, Institute of Botany, University of Neuchâtel, Rue Émile-Argand 11, Case Postale 158, 2009 Neuchâtel, Switzerland;,
Departamento de Ciencias Agrarias y del Medio Natural, Área de Fisiología Vegetal, Universitat Jaume I, Borriol s/n, 12071 Castellón, Spain;, and
Section of Phytopathology, Faculty of Biology, Utrecht University, PO Box 80084, 3508 TB Utrecht, The Netherlands
Abstract: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.
Keywords:BABA  PMR4  ABA  induced resistance  callose  JA
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