The vesicular trafficking system component MIN7 is required for minimizing Fusarium graminearum infection

Abstract

Abstract Plants have developed intricate defense mechanisms, referred to as innate immunity, to defend themselves against a wide range of pathogens. Plants often respond rapidly to pathogen attack by the synthesis and delivery to the primary infection sites of various antimicrobial compounds, proteins, and small RNA in membrane vesicles. Much of the evidence regarding the importance of vesicular trafficking in plant–pathogen interactions comes from studies involving model plants whereas this process is relatively understudied in crop plants. Here we assessed whether the vesicular trafficking system components previously implicated in immunity in Arabidopsis play a role in the interaction with Fusarium graminearum, a fungal pathogen well-known for its ability to cause Fusarium head blight disease in wheat. Among the analysed vesicular trafficking mutants, two independent T-DNA insertion mutants in the AtMin7 gene displayed a markedly enhanced susceptibility to F. graminearum. Earlier studies identified this gene, encoding an ARF-GEF protein, as a target for the HopM1 effector of the bacterial pathogen Pseudomonas syringae pv. tomato, which destabilizes MIN7 leading to its degradation and weakening host defenses. To test whether this key vesicular trafficking component may also contribute to defense in crop plants, we identified the candidate TaMin7 genes in wheat and knocked-down their expression through virus-induced gene silencing. Wheat plants in which TaMin7 genes were silenced displayed significantly more Fusarium head blight disease. This suggests that disruption of MIN7 function in both model and crop plants compromises the trafficking of innate immunity signals or products resulting in hypersusceptibility to various pathogens.