Mauch-Mani, Brigitte

2007, Ton, Jurriaan, D'Alessandro, Marco, Jourdie, Violaine, Jakab, Gabor, Karlen, Danielle, Held, Matthias, Mauch-Mani, Brigitte, Turlings, Ted

Plants counteract attack by herbivorous insects using a variety of inducible defence mechanisms. The production of toxic proteins and metabolites that instantly affect the herbivore's development are examples of direct induced defence. In addition, plants may release mixtures of volatile organic compounds (VOCs) that indirectly protect the plant by attracting natural enemies of the herbivore. Recent studies suggest that these VOCs can also prime nearby plants for enhanced induction of defence upon future insect attack. However, evidence that this defence priming causes reduced vulnerability to insects is sparse. Here we present molecular, chemical and behavioural evidence that VOC-induced priming leads to improved direct and indirect resistance in maize. A differential hybridization screen for inducible genes upon attack by Spodoptera littoralis caterpillars identified 10 defence-related genes that are responsive to wounding, jasmonic acid (JA), or caterpillar regurgitant. Exposure to VOCs from caterpillar-infested plants did not activate these genes directly, but primed a subset of them for earlier and/or stronger induction upon subsequent defence elicitation. This priming for defence-related gene expression correlated with reduced caterpillar feeding and development. Furthermore, exposure to caterpillar-induced VOCs primed for enhanced emissions of aromatic and terpenoid compounds. At the peak of this VOC emission, primed plants were significantly more attractive to parasitic Cotesia marginiventris wasps. This study shows that VOC-induced priming targets a specific subset of JA-inducible genes, and links these responses at the molecular level to enhanced levels of direct and indirect resistance against insect attack.

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.

2004, Ton, Jurriaan, Mauch-Mani, Brigitte

The non-protein amino acid β-amino-butyric acid (BABA) protects plants against a wide range of pathogens. We have examined the effectiveness and mode of action of BABA on resistance against two necrotrophic pathogens. Treatment of Arabidopsis with BABA induced resistance against Alternaria brassicicola and Plectosphaerella cucumerina to a similar level by jasmonic acid (JA). Conversely, treatment with benzothiadiazole (BTH), a functional analogue of salicylic acid (SA), had no significant effect on the resistance against both pathogens. BABA-induced resistance against A. brassicicola and P. cucumerina was unaffected in the JA-insensitive mutant coi1-1 and the camalexin-deficient mutant pad3-1. Moreover, the expression of BABA-induced resistance was not associated with enhanced accumulation of camalexin or enhanced transcription of the JA-inducible PDF1.2 gene. The expression of BABA-induced resistance against P. cucumerina was unaffected in mutants impaired in ethylene (ET) and SA signalling, but was blocked in the abscisic acid (ABA)-deficient mutant aba1-5, the ABA-insensitive mutant abi4-1 and the callose-deficient mutant pmr4-1. Upon infection by both pathogens, BABA-treated plants showed an earlier and more pronounced accumulation of callose. Treatment with the callose-inhibitor 2-deoxy-D-glucose (2-DDG) reversed the BABA-induced resistance against A. brassicicola. Furthermore, primed callose deposition was absent in BABA-treated abi4-1 and pmr4-1 plants upon infection by P. cucumerina. Although the expression of BABA-induced resistance was not associated with enhanced transcription of the ABA-inducible RAB18 gene, application of ABA mimicked the effect of BABA on the level of callose accumulation and resistance. Hence, BABA-induced resistance against necrotrophic pathogens is based on primed callose accumulation, which is controlled by an ABA-dependent defence pathway.