Rhynchosporium commune effectors and their potential role during barley colonisation

Anna Avrova Louise Gamble Lucie Griffe Kathryn Ford Dimitar Epihov
Cell and Molecular Sciences, James Hutton Institute, Dundee, UK

For over a century Rhynchosporium commune has remained one of the most destructive and economically important pathogens of barley. R. commune is a hemibiotroph with a prolonged asymptomatic phase. Following conidia germination on the leaf surface and cuticle penetration, fungal hyphae spread between the host epidermal cells without directly penetrating them.

Sequencing of the R. commune genome, and transcriptomes from germinated conidia and an early time point during barley infection, led to identification of putative effectors with roles in the interaction with the host plant. Some of the identified effectors, including a secreted chorismate mutase and a family of LysM domain proteins, may be responsible for the delay in symptoms development. The R. commune genome contains an extended family of genes encoding proteins with one or more LysM domains. LysM1, LysM5 and LysM7 contain just one LysM domain, while LysM2 - two domains, LysM3 - three domains, LysM4 and LysM6 - four domains. In addition, two genes code for enzymes containing LysM domain pairs, a subgroup C chitinase, which also contains a different chitin-binding motif, and a putative peptidoglycan lytic transglycosidase. Transcriptional upregulation of R. commune secreted chorismate mutase and several genes encoding LysM domain proteins at the start of barley colonisation suggests their importance during the early stages of interaction with the host. The ability of LysM2 and LysM3 produced using Pichia pastoris to bind chitin and chitosan suggest their role in prevention of the host immune response to chitin. Chorismate mutase on the other hand might be involved in manipulation of SA mediated defences in barley resulting in a compatible interaction. Targeted gene silencing of candidate effectors will help to determine their importance for pathogenicity.