Article ID: 17.0501a
The obligate biotrophic fungal pathogens that cause powdery mildew disease establish infection in living host cells by modifying host cellular functions, including membrane trafficking. Previously, we reported that two Arabidopsis thaliana RAB5 GTPases, plant-specific ARA6/RABF1 and canonical ARA7/RABF2b, accumulate at the extrahaustorial membrane (EHM), which surrounds the specialized infection hypha called the haustorium. In this study, we examined the role of ARA6 and ARA7, which regulate distinctive endosomal trafficking pathways, in plant–powdery mildew fungus interactions. Although ARA6- and ARA7-related mutants did not exhibit altered susceptibility to the A. thaliana–adapted powdery mildew fungus Golovinomyces orontii, overexpression of constitutively active ARA6, but not constitutively active ARA7, repressed proliferation of G. orontii. The repression of fungal proliferation was associated with accelerated formation of the callosic encasement around the haustorium. Furthermore, microscopic observation revealed an accumulation of the constitutively active form of ARA6, but not active ARA7, at the EHM. These results indicate that plant-specific ARA6 has a specific role in plant–powdery mildew fungus interaction, and manipulation of ARA6 activity could be a novel tool to overcome this plant disease.