Flors, Victor

2008, Flors, Victor, Ton, Jurriaan, Van Doorn, Ronald, Jakab, Gabor, García-Agustín, Pilar, Mauch-Mani, Brigitte

2006, Conrath, Uwe, Beckers, Gerold J. M., Flors, Victor, García-Agustín, Pilar, Jakab, Gábor, Mauch, Felix, Newman, Mari-Anne, Pieterse, Corné M. J., Poinssot, Benoit, Pozo, María J., Pugin, Alain, Schaffrath, Ulrich, Ton, Jurriaan, Wendehenne, David, Zimmerli, Laurent, Mauch-Mani, Brigitte

Infection of plants by necrotizing pathogens or colonization of plant roots with certain beneficial microbes causes the induction of a unique physiological state called “ priming”. The primed state can also be induced by treatment of plants with various natural and synthetic compounds. Primed plants display either faster, stronger, or both activation of the various cellular defense responses that are induced following attack by either pathogens or insects or in response to abiotic stress. Although the phenomenon has been known for decades, most progress in our understanding of priming has been made over the past few years. Here, we summarize the current knowledge of priming in various induced-resistance phenomena in plants.

2007, Flors, Victor, Ton, Jurriaan, van Doorn, Ronald, Jakab, Gabor, García-Agustín, 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.

2006, Conrath, Uwe, Beckers, Gerold J. M., Flors, Victor, García-Agustín, Pilar, Jakab, Gábor, Mauch, Felix, Newman, Mari-Anne, Pieterse, Corné M. J., Poinssot, Benoit, Pozo, María J., Pugin, A., Schaffrath, U., Ton, Jurriaan, Wendehenne, D., Zimmerli, L., Mauch-Mani, Brigitte