Copper Tolerance Mediated By FgAceA And FgCrpA In Fusarium Graminearum

All organisms must secure essential trace elements for survival and reproduction.However,excess trace element accumulation in cells is highly toxic.The maintenance of copper(Cu)homeostasis has been extensively studied in mammals,bacteria,and yeast but not in plant pathogens.In this study,we investigated the molecular mechanisms of copper tolerance in Fusarium graminearum,the important wheat head scab fungus.RNA-Seq revealed induced expression of the P-type ATPase transporter FgCrpA and metallothionein(MT)FgCrdA after excess Cu treatment.Deletion of FgCrpA but not FgCrdA resulted in reduced Cu toxicity tolerance.The“Cu fist”transcription factor FgAceA was involved in Cu detoxification through activation of the P-type ATPase transporter FgCrpA.?FgAceA was more sensitive to copper toxicity than ?FgCrpA.FgAceA negatively regulated aurofusarin production and aurofusarin biosynthesis gene expression.The induced expression of FgCrpA under excess Cu treatment was alleviated in?FgAceA,and overexpression of FgCrpA restored copper tolerance in?FgAceA.Reduced virulence in flowering wheat heads and decreased accumulation of the toxic metabolite deoxynivalenol(DON)in?FgCrpA and?FgAceA were observed when mutants were challenged with excess Cu.The above experimental results show that mediation of Cu tolerance in F.graminearum mainly relies on the Cu efflux pump and that FgAceA governs Cu detoxification through activation of FgCrpA.Under the excess Cu²⁺,FgAceA and FgCrpA play a crucial role in the growth and development,toxin synthesis and pathogenicity of F.graminearum,providing a theoretical basis for the search for the control methods of F.graminearum.