Interplay between JA, SA and ABA isgnalling during basal and induced resistance against pseudomonas syringae and Alternaria brasicicola
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Otros documentos de la autoría: Jakab, Gabor; García Agustín, Pilar; Mauch-Mani, Brigitte; Ton, Jurriaan; Van Doorn, Ronald; Flors, Victor
Metadatos
Mostrar el registro completo del ítemcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/2508
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INVESTIGACIONMetadatos
Título
Interplay between JA, SA and ABA isgnalling during basal and induced resistance against pseudomonas syringae and Alternaria brasicicolaAutoría
Fecha de publicación
2008Editor
Wiley-BlackwellISSN
0960-7412Cita bibliográfica
FLORS, Victor, et al. Interplay between JA, SA and ABA signalling during basal and induced resistance against Pseudomonas syringae and Alternaria brassicicola. The Plant Journal, 2008, vol. 54, no 1, p. 81-92.Tipo de documento
info:eu-repo/semantics/articleVersión de la editorial
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-313X.2007.03397.xPalabras clave / Materias
Resumen
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 ... [+]
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. [-]
Publicado en
The Plant journal; vol. 54, núm. 1Derechos de acceso
http://rightsstatements.org/vocab/CNE/1.0/
info:eu-repo/semantics/openAccess
info:eu-repo/semantics/openAccess
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