Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/11/2019
Publication Date: 2/13/2019
Citation: Hao, G., McCormick, S., Vaughan, M.M., Naumann, T.A, Kim, H.-S., Proctor, R., Kelly, A., Ward, T.J. 2019. Fusarium graminearum arabinanase (Arb93B) enhances wheat head blight susceptibility by suppressing plant immunity. Molecular Plant-Microbe Interactions. https://doi.org/10.1094/MPMI-06-18-0170-R.
Interpretive Summary: Fusarium head blight (FHB) caused by the fungus Fusarium graminearum is one of the most devastating diseases of wheat and other cereals. In addition, FHB results in contamination of grain with fungal toxins, known as mycotoxins that can be a serious threat to food safety and animal health. In order to reduce the incidence of FHB and mycotoxin contamination of grain, we need to understand how Fusarium interacts with plant and overcomes plant defenses to cause disease. In this study, we discovered that a Fusarium protein Arb93B plays an important role in FHB development in wheat. Arb93B was identified as an arabinanase, indicating that it may be involved in degrading plant cell walls during infection. In addition, we also demonstrated that Arb93B reduced key components of the plant immune response to fungal invasion. This study helps us further understand pathogen and plant interactions during infection, and provides an important information for the development of novel methods to control FHB and mycotoxin contamination.
Technical Abstract: Fusarium head blight (FHB) of wheat and barley caused by the fungus Fusarium graminearum reduces crop yield and contaminates grain with mycotoxins. In this study, we investigated two exo-1, 5-a-L-arabinanases (Arb93A and Arb93B) secreted by F. graminearum, and their effect on wheat head blight development. Arabinan is an important component of plant cell walls, but it was not known if these arabinanases play a role in FHB. Both ARB93A and ARB93B were induced during the early stages of infection. arb93A mutants did not exhibit a detectable change in ability to cause FHB, whereas, arb93B deletion mutants caused lower levels of FHB symptoms and deoxynivalenol contamination compared to the wild type. Furthermore, virulence and deoxynivalenol contamination were restored to wild-type levels in ARB93B complemented mutants. Fusion proteins of GFP with the predicted chloroplast peptide or the mature protein of Arb93B were not observed in the chloroplast. Reactive oxygen species production was reduced in the infiltrated zones of N. benthamiana leaves expressing ARB93B. Co-expression of ARB93B and Bax in N. benthamiana leaves significantly suppressed Bax-programmed cell death. Our results indicate that Arb93B enhances plant disease susceptibility by suppressing ROS associated plant defense responses.