The Populus species possess great potential for therapeutical applications, especially for their known anti-inflammatory properties. The antioxidant properties of propolis, a hive product collected by honey bees mainly from poplar bud exudates, suggest that poplar buds also possess antioxidant properties. Here is reported the characterization of the antioxidant properties of an aqueous poplar bud (Populus nigra) extract. It presented a high total phenolic content, and moderate antioxidant properties as determined by ORAC assay. The main phenolic compounds identified were phenolic acids and flavonoid aglycons. These phenolic compounds were analyzed by ORAC assay for their individual antioxidant activity, in order to determine the major contributors to the total antioxidant activity of the extract. Thanks to their high antioxidant activity, caffeic and p-coumaric acids were identified as the major antioxidant components. Representing only 3.5% of its dry weight, these compounds represented together about 50% of the total antioxidant activity of the extract. The antioxidant properties of poplar bud extract and the phenolic compounds identified were also analyzed by cellular antioxidant activity assay (CAA), which was weakly correlated with ORAC assay. The transcriptional effect of poplar bud extract on skin aging was evaluated in vitro on a replicative senescence model of normal human dermal fibroblasts, using a customized DNA macroarray specifically designed to investigate skin aging markers. Among the detected genes, poplar bud extract significantly regulated genes involved in antioxidant defenses, inflammatory response and cell renewal. The collective antioxidant properties and transcriptional effect of this extract suggest potential antiaging properties which could be utilized in cosmetic and nutraceutical formulations.

SummaryCamalexin, the characteristic phytoalexin of Arabidopsis thaliana, inhibits growth of the fungal necrotroph Alternaria brassicicola. This plant metabolite probably exerts its antifungal toxicity by causing cell membrane damage. Here we observed that activation of a cellular response to this damage requires cell wall integrity (CWI) and the high osmolarity glycerol (HOG) pathways. Camalexin was found to activate both AbHog1 and AbSlt2 MAP kinases, and activation of the latter was abrogated in a AbHog1 deficient strain. Mutant strains lacking functional MAP kinases showed hypersensitivity to camalexin and brassinin, a structurally related phytoalexin produced by several cultivated Brassica species. Enhanced susceptibility to the membrane permeabilization activity of camalexin was observed for MAP kinase deficient mutants. These results suggest that the two signalling pathways have a pivotal role in regulating a cellular compensatory response to preserve cell integrity during exposure to camalexin. AbHog1 and AbSlt2 deficient mutants had reduced virulence on host plants that may, at least for the latter mutants, partially result from their inability to cope with defence metabolites such as indolic phytoalexins. This constitutes the first evidence that a phytoalexin activates fungal MAP kinases and that outputs of activated cascades contribute to protecting the fungus against antimicrobial plant metabolites.

SummaryThe unfolded protein response (UPR) is an important stress signalling pathway involved in the cellular development and environmental adaptation of fungi. We investigated the importance of the UPR pathway in the pathogenicity of the plant necrotrophic fungus Alternaria brassicicola, which causes black spot disease on a wide range of Brassicaceae. We identified the AbHacA gene encoding the major UPR transcription regulator in A. brassicicola. Deletion of AbHacA prevented induction of the UPR in response to endoplasmic reticulum stress. Loss of UPR in mutants resulted in a complete loss of virulence and was also associated with a cell wall defect and a reduced capacity for secretion. In addition, our results showed that the UPR was triggered by treatment of mycelia with camalexin, i.e. the major Arabidopsis thaliana phytoalexin, and that strains lacking functional AbHacA exhibited increased in vitro susceptibility to antimicrobial plant metabolites. We hypothesize that the UPR plays a major role in fungal virulence by altering cell protection against host metabolites and by reducing the ability of the fungus to assimilate nutrients required for growth in the host environment. This study suggests that targeting the UPR pathway would be an effective plant disease control strategy.

No abstract