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Plant microbiota appear more and more as potential sources of antagonistic microorganisms. However, the seed microbiota associated with wild plant species has rarely been explored. To identify fungal antagonists to the seed-borne pathogen Alternaria brassicicola, seeds were collected in natural populations of three Brassicaceae species, Arabidopsis thaliana, Capsella bursa-pastoris and Draba verna. A large number of fungal strains reduced the growth of A. brassicicola. The most antagonistic strains belonged to Alternaria, Apiospora, Trichoderma and Aspergillus. Seed-associated fungi tolerated host plant defenses and exhibited lower sensitivity compared to A. brassicicola to indolic compounds such as the phytoalexin camalexin and the glucosinolates (GLS)-breakdown compound indole-3-carbinol. By contrast, antagonistic strains were as inhibited as A. brassicicola in presence of allyl-isothiocyanates (ITC) derived from aliphatic GLS, and more inhibited by benzyl-ITC derived from aromatic GLS. However, all defense compounds could enhance the antagonistic effects of some of the isolated strains on A. brassicicola. The observed potential synergistic effects between defense compounds and seed-associated antagonistic strains emphasize the need for further studies to elucidate the molecular bases of the interactions. A better understanding of the interactions between host plants, pathogens and fungal endophytes is also needed to develop sustainable biocontrol strategies.

Acibenzolar-S-methyl (ASM) is a chemical compound, which is able to induce resistance in several model and non-model plants, but the end-players of this induced defense remain ill-defined. Here, we test the hypothesis that treatment with ASM can protect apple (Malus × domestica) against the rosy apple aphid (Dysaphis plantaginea) and investigate the defense molecules potentially involved in resistance. We measured aphid life traits and performed behavioral assays to study the effect of ASM on plant resistance against the aphid, and then combined transcriptomic, bioinformatics, metabolic and biochemical analyses to identify the plant compounds involved in resistance. Plants treated with ASM negatively affected several life traits of the aphid and modified its feeding and host seeking behaviors. ASM treatment elicited up-regulation of terpene synthase genes in apple and led to the emission of (E,E)-α-farnesene, a sesquiterpene that was repellent to the aphid. Several genes encoding amaranthin-like lectins were also strongly up-regulated upon treatment and the corresponding proteins accumulated in leaves, petioles and stems. Our results link the production of specific apple proteins and metabolites to the antibiosis and antixenosis effects observed against Dysaphis plantaginea, providing insight into the mechanisms underlying ASM-induced herbivore resistance.