The Study Of Fungicide Sensitivity Regulated By Transcription Factor FgTeb And Microtubule-associated Protein FgEB1 In Fusarium Garminearum

The target of benzimidazole is microtubule and the amino acid mutations in?2-tubulin causes the resistance to carbendazim in Fusarium graminearum.DMIs fungicide could inhibit the activity of the sterol 14-?-demethylase which is the key enzyme in ergosterol biosynthesis.That the DMIs resistance of plant and animal fungal pathogens have been widely reported.JS399-19 is a novel fungicide to control the FHB(Fusarium head blight),and its target is myosin I in F.graminearum.Recently studies showed that the UV could induce the mutation in myosinl and led to resistance to JS399-19 which indicates the high resistant risk of the fungicide.This study focused on two kinds of proteins which regulate the sensitivity to these fungicides in F.graminearum,and the major results showed that:1.We found the FgTeb could bind the promoter of FgCYP51A gene to regulate the sensitivity to DMIs and ergosterol biosynthesis in F.graminearum.In addition,the phenomenon that DMIs could induce the expression of FgCYP51A was disappeared in the ?FgTEB.The ChIP-seq results show that the FgTeb could bind the promoter of 19 genes in ergosterol biosynthesis pathway,and regulates the expression of these genes.We identified the motif that bound by the FgTeb using the Y1H and in situ complemented assays.Moreover,the ?FgTEB showed hypersensitive to phytolexin and produced the less DON compared the wild type,which led to the reduced virulence of FgTeb on wheat head.2.The end binding protein FgEB1 could form different complex with different proteins to regulate the development of cellular polarity and resistance to cabendazim or JS19-399.The FgEB1 mutants of F.graminearum exhibits twisted hyphae,increased hyphal branching and curved conidia.Using the affinity capture,we identified four core septins as FgEB1 interacting proteins,and found that FgEB1 and septins regulated conidial polar growth in the opposite orientation.Interestingly,FgEB1 and FgKar9 constituted another complex that modulated the response to cabendazim,amicrotuble-damaging agent specifically.In addition,the lack of FgEB1 altered the distribution of polarity-related classed 1 myosin via interaction with the actin.