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Fusarium  head blight caused by  Fusarium graminearum  is an important disease of wheat and barley. Previous studies have showed that all three MAP kinase genes,  MGV1, FgHOG1 , and  GPMK1 , are involved in regulating hyphal growth, sexual reproduction, plant infection, and stress responses in this pathogen. To determine the relationship between the Mgv1 and FgHog1 pathways, in this study, we generated and characterized the  mgv1 Fghog1  double mutant. Deletion of  FgHOG1  partially rescued the defects of the  mgv1  mutant in vegetative growth and cell wall integrity but had no effects on its defects in plant infection and DON production. The  mgv1 Fghog1  mutant grew faster and was more tolerant to cell wall stressors than the  mgv1  mutant. Swollen compartments and cell burst were observed frequently in the  mgv1  mutant but rarely in the  mgv1 Fghog1  mutant when treated with fungicide fludioxonil or cell wall stressor Congo red. Conversely, the deletion of  MGV1  also alleviated the hyperosmotic sensitivity of the  Fghog1  mutant in vegetative growth. TGY assays indicated increased phosphorylation of FgHog1 in the  mgv1  mutant, and TEY assays further revealed elevated activation of Gpmk1 in the  mgv1 Fghog1  double mutant, particularly under cell wall stress conditions. Overall, our data showed that deletion of  FgHOG1  partially suppressed the defects of the  mgv1  mutant, possibly by affecting genes related to cell wall integrity and osmoregulation  via  the over-activation of Gpmk1 MAP kinase and avoiding intracellular turgor elevation.

frontiers in microbiology

Deletion of FgHOG1 Is Suppressive to the mgv1 Mutant by Stimulating Gpmk1 Activation and Avoiding Intracellular Turgor Elevation in Fusarium graminearum