All organisms must secure essential trace elements (e.g., Cu) 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 tolerance to Cu toxicity. The “Cu fist” transcription factor FgAceA was involved in Cu detoxification through activation of FgCrpA. △FgAceA was more sensitive to copper toxicity than △FgCrpA and overexpression of FgCrpA restored copper tolerance in △FgAceA. FgAceA negatively regulated aurofusarin production and its biosynthetic gene expression. △FgCrpA and △FgAceA were reduced in virulence in flowering wheat heads and synthesized decreased amounts of the mycotoxin deoxynivalenol when challenged with excess Cu. Taken together, these results suggest 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.

所有生物都必须确保生存和繁殖所必需的微量元素（例如Cu）。然而，细胞中过量的微量元素积累是剧毒的。铜（Cu）稳态的维持已在哺乳动物，细菌和酵母中进行了广泛研究，但在植物病原体中并未进行。在这项研究中，我们研究了铜耐性的分子机制。禾谷镰刀菌，重要的小麦头sc真菌。RNA序列显示诱导表达的P型ATPase转运蛋白。FgCrpA 和金属硫蛋白（MT） FgCrdA经过过量的铜处理。删除FgCrpA 但不是 FgCrdA导致对铜毒性的耐受性降低。“铜拳头”转录因子FgAceA通过激活铜而参与了铜的解毒。FgCrpA。△FgAceA对铜的毒性比△FgCrpA更敏感，并且过表达FgCrpA 恢复△FgAceA的铜公差。 FgAceA负调控的aurofusarin生产及其生物合成基因的表达。过量的Cu攻击后，开花的小麦头中的△FgCrpA和△FgAceA的毒力降低，并且合成的霉菌毒素脱氧雪腐酚含量降低。综上所述，这些结果表明，在禾本科 主要依靠铜外排泵 FgAceA 通过激活铜来控制铜的解毒 FgCrpA。