The sucrose non-fermenting-1 kinase Snf1 is involved in fludioxonil resistance via interacting with the high osmolarity glycerol MAPK kinase Hog1 in Fusarium

Abstract

Abstract Fusarium head blight (FHB) caused by Fusarium graminearum complex is a worldwide devastating disease of wheat, barley, maize, and other cereals. In the field, application of fungicides is one of the main strategies for management of FHB. With the long-time usage of fungicides, resistant pathogen populations have become a new challenge for disease management. Application of new pesticide is necessary for sustainable control of this disease. The phenylpyrrole fungicide fludioxonil has been registered recently for management of FHB. However, the resistance mechanisms of F. graminearum to this compound are largely unknown. Here we isolated a biocontrol bacterium Burkholderia pyrrocina W1, which produced the antifungal compound pyrrolnitrin and showed greatly antagonistic activity towards FHB. Spontaneous mutants of pyrrolnitrin-resistant F. graminearum were induced and re-sequenced. Single base mutations were identified in the genes encoding the osmoregulation MAP kinase Hog1 and the AMP dependent kinase Snf1 in pyrrolnitrin-resistant mutants. Snf1 was further confirmed to interact with Hog1 and involved in the response of this fungus to pyrrolnitrin and its derivate, the fungicide fludioxonil. This study reveals that the Snf1 interacts with Hog1 to regulate fludioxonil resistance in a pathogenic fungus.

Keywords

• Fusarium graminearum
• Pyrrolnitrin
• Fludioxonil
• Fungicide resistance
• HOG pathway
• Snf1 kinase