Abstract
ABSTRACTZymoseptoria triticiis an ascomycete fungus and the causal agent of Septoria tritici leaf blotch (STB) in wheat.Z. triticisecretes an array of effector proteins that are likely to facilitate host infection, colonisation and pycnidia production. In this study we demonstrate a role for Zt-11 as aZ. triticieffector during disease progression.Zt-11is upregulated during the transition of the pathogen from the biotrophic to necrotrophic phase of wheat infection. Deletion ofZt-11delayed disease development in wheat, reducing the number and size of pycnidia, as well as the number of macropycnidiospores produced byZ. tritici. This delayed disease development by the ΔZt-11mutants was accompanied by a lower induction ofPRgenes in wheat, when compared to infection with wildtypeZ. tritici. Overall, these data suggest that Zt-11 plays a role inZ. triticiaggressiveness and STB disease progression possibly via a salicylic acid associated pathway.
Publisher
Cold Spring Harbor Laboratory