Summary• Botrytis cinerea is a necrotrophic pathogen that attacks more than 200 plant species.• Here, the nonpathogenic mutant A336, obtained via insertional mutagenesis, was characterized.• Mutant A336 was nonpathogenic on leaves and fruits, on intact and wounded tissue, while still able to penetrate the host plant. It grew normally in vitro on rich media but its conidiation pattern was altered . The mutant did not produce oxalic acid and exhibited a modified regulation of the production of some secreted proteins (acid protease 1 and endopolygalacturonase 1). Culture filtrates of the mutant triggered an important oxidative burst in grapevine ( Vitis vinifera ) suspension cells, and the mutant-plant interaction resulted in the formation of hypersensitive response-like necrosis. Genetic segregation analyses revealed that the pathogenicity phenotype was linked to a single locus, but showed that the mutated gene was not tagged by the plasmid pAN7-1.• Mutant A336 is the first oxalate-deficient mutant to be described in B. cinerea and it differs from all the nonpathogenic B. cinerea mutants described to date.

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In plant/parasitic plant interaction, little is known about the host plant response before the establishment of the parasite within the host. In the present work, we focused on host responses to parasitic plant, O. ramosa in the early stage of infection. We used a co-culture system of A. thaliana suspension cells and O. ramosa germinated-seeds to avoid parasite attachment. We showed that O. ramosa induced H 2 O 2 generation and camalexin synthesis by A. thaliana followed by a drastic increase in cell death. We further demonstrated that a heat sensitive diffusible signal is responsible for this cell death. These data indicate that recognition of O. ramosa occurs before the attachment of the parasite and initiates plant defence responses.