Flors, Victor

2014, Pastor, Victoria, Pena, Andrea, Gamir, Jordi, Flors, Victor, Mauch-Mani, Brigitte

2012, Slaughter, Ana, Daniel, Xavier, Flors, Victor, Luna, Estrella, Hohn, Barbara, Mauch-Mani, Brigitte

2009, Ton, Jurriaan, Flors, Victor, Mauch-Mani, Brigitte

Long known only for its role in abiotic stress tolerance, recent evidence shows that abscisic acid (ABA) also has a prominent role in biotic stress. Although it acts as a negative regulator of disease resistance, ABA can also promote plant defense and is involved in a complicated network of synergistic and antagonistic interactions. Its role in disease resistance depends on the type of pathogen, its specific way of entering the host and, hence, the timing of the defense response and the type of affected plant tissue. Here, we discuss the controversial evidence pointing to either a repression or a promotion of resistance by ABA. Furthermore, we propose a model in which both possibilities are integrated.

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.

2014, Boachon, Benoît, Gamir, Jordi, Pastor, Victoria, Erb, Matthias, Dean, John V., Flors, Victor, Mauch-Mani, Brigitte

2012, Pastor, Victoria, Vicent, Cristian, Cerezo, Miguel, Mauch-Mani, Brigitte, Dean, John, Flors, Victor

2009, Mauch-Mani, Brigitte, Flors, Victor

2013, Balmer, Dirk, Flors, Victor, Glauser, Gaetan, Mauch-Mani, Brigitte

2009, Mauch-Mani, Brigitte, Flors, Victor

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