Mechanisms Of The HOG-MAPK Pathway In Regulating Fusarium Graminearum Sensitivity To Triazole Fungicides

Wheat scab is a destructive disease,which mainly relies on chemical control in production.As a result of large-scale use for a long time,the problem of drug resistance is becoming increasingly prominent.A component of resistance of Fusarium graminearum-the transcription factor FgSR,which regulates ergosterol biosynthesis,was found earlier in this study.Therefore,we mainly focus on the transcription factor FgSR to study the regulation mechanism of sterol synthesis in Fusarium graminearum.In order to find potential interacting proteins of transcription factor FgSR,we screened a candidate kinase FgSsk2 from Fusarium graminearum cDNA library and yeast double hybrid screening library.Further studies showed that the knockout mutant of FgSsk2(AFgSsk2)was more sensitive to tebuconazole,and the expression of FgCYP51A gene in the mutant decreased significantly.FgSsk2 is a component of the kinase cascade in the HOG-MAPK pathway.The other two FgPbs2 and FgHog1 knockout mutants downstream of FgSsk2 have the same tebuconazole-sensitive phenotype as AFgSsk2.After treatment with tebuconazole,the phosphorylation level of kinase FgHog1 increased,and the localization of kinase FgHog1 in nucleus increased significantly.The phosphorylation of transcription factor FgSR in the single knock mutants of three kinases decreased significantly,and FgSsk2 controlled the phosphorylation of downstream kinase FgHogl,which interacted with the transcription factor FgSR.These results suggest that tebuconazole treatment activates the HOG-MAPK pathway,activated FgHogl will enter the nucleus and phosphorylate FgSR to regulate FgCYP51A expression.In this study,HOG-MAPK signaling pathway regulates the expression of tebuconazole drug target gene FgCYP51A through phosphorylation transcription factor FgSR.