Molecular Mechanisms Of Iron Excess Adaptation In Fusarium Graminearum During Infection

Iron is an important tranc element,and the balance of iron homeostasis plays an important role in oxygen transport,electron transport and enzyme activation.Plant pathogens are challenged by host-derived iron starvation or iron excess during infection.Successful infection of plant pathogens needs to overcome the iron stress,However the mechanism through which pathogens counteract iron stress is unclear.In fungi,iron homeostasis is primarily maintained via transcriptional regulation by two transcription factors HapX and SreA:HapX is responsible for iron utilizating and storaging;SreA regulates iron acquisition.Histone modification,histone variant or chromatin remodeling complex can regulate chromatin structure.At present,the effect of chromatin structure changes on iron homeostasis genes expression has not been fully characterized.Fusarium head blight(FHB)caused by the plant pathogen Fusarium graminearum is a devastating disease.In addition to yield loss,this pathogen also contaminates grains with mycotoxins,such as deoxynivalenol and zearalenone,which pose a great threat to human and animal health.In this study,the mechanism in F.graminearum counteracting iron stress was discussed,which is helpful to understand the host adaptability of F.graminearum and provide a theoretical basis for the prevention and control of FHB.In this study,we found that F.graminearum encounters host-derived iron excess during infection.Next,we uncovered the molecular mechanisms of iron excess adaptation using genetic transformation,in vivo or in vitro proteins interaction assay,RNA-sequencing,Chromatin immunoprecipitation(ChIP)-sequencing,ChIP-q PCR and other methods.1)Deletion of iron homeostasis transcription factors FgHapX,FgSreA or both attenuated virulence.Deletion of FgHapX led to the imbalance of iron homeostasis genes,deletion of FgSreA led to upregulate iron acquisition genes,which indicates that both of FgHapX and FgSreA were involved in the response to iron excess during infection.2)FgHapX derepresses iron utilization genes and FgSREA via dissociation from their promoters under iron excess treatment.Meantime,FgHapX enhances histone H2 B deubiquitination(H2B deub1)in the promoter of FgCCCA to activate iron storage upon iron excess.3)FgSreA promotes the deposition of histone variant H2 A.Z and the H3K27 me3 level at iron uptake genes to decrease transcription under iron excess.4)The monothiol glutaredoxin FgGrx4 is responsible for iron sensing and control of the transcriptional activity of FgHapX and FgSreA via modulation of their enrichment at target genes and recruitment of epigenetic regulators,respectively.Taken together,our findings elucidate the molecular mechanisms for adaptation to iron excess mediated by FgHapX and FgSreA during infection in F.graminearum and provide novel insights into regulation of iron homeostasis at the chromatin level in eukaryotes.