Mechanism of validamycin A inhibiting DON biosynthesis and synergizing with DMI fungicides against Fusarium graminearum.
Mechanism of validamycin A inhibiting DON biosynthesis and synergizing with DMI fungicides against Fusarium graminearum.
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井冈霉素A抑制DON生物合成并与DMI杀菌剂协同抗禾谷镰刀菌的作用机制。
DOI：
10.1111/mpp.13060
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发表时间：
2021-07
影响因子：
4.9
通讯作者：
Zhou M
中科院分区：
文献类型：
--
作者：
Bian C;Duan Y;Xiu Q;Wang J;Tao X;Zhou M
摘要脱氧雪腐镰刀菌醇（脱氧雪腐镰刀菌醇，DON）是引起赤霉病（Fusarium head blight， FHB）的重要毒力因子。我们最近发现一种氨基糖苷类抗生素validamycin A （VMA）可用于控制FHB和抑制DON污染，但其分子机制尚不清楚。在本研究中，我们发现中性海藻化酶和酸性海藻化酶（FgNTH和FgATH）都是fma的靶点，FgNTH和FgATH的缺乏使VMA的敏感性分别降低了2.12倍和1.79倍，表明FgNTH是VMA的主要靶点。我们发现FgNTH负责营养生长，FgATH对有性生殖至关重要，两者在F. graminearum的分生和毒力中都起重要作用。我们发现FgNTH存在于细胞质中，影响FgATH的定位，并积极调节DON的生物合成；然而，FgATH驻留在液泡中，负调控DON的生物合成。FgNTH与糖酵解关键酶丙酮酸激酶（FgPK）相互作用，VMA降低了这种相互作用；在DON诱导条件下，FgNTH缺乏影响FgPK的定位。缺乏FgNTH的菌株对去甲基化抑制剂（DMI）杀菌剂更敏感。FgNTH通过与FgCYP51B相互作用调节FgCYP51A和FgCYP51B的表达水平。综上所述，VMA通过靶向FgNTH并减少FgNTH与FgPK之间的相互作用来抑制DON的生物合成，并通过降低FgCYP51A和FgCYP51B的表达与DMI杀菌剂协同作用来对抗F. graminearum。
Abstract Deoxynivalenol (DON) is a vital virulence factor of Fusarium graminearum, which causes Fusarium head blight (FHB). We recently found that validamycin A (VMA), an aminoglycoside antibiotic, can be used to control FHB and inhibit DON contamination, but its molecular mechanism is still unclear. In this study, we found that both neutral and acid trehalase (FgNTH and FgATH) are the targets of VMA in F. graminearum, and the deficiency of FgNTH and FgATH reduces the sensitivity to VMA by 2.12‐ and 1.79‐fold, respectively, indicating that FgNTH is the main target of VMA. We found FgNTH is responsible for vegetative growth, FgATH is critical to sexual reproduction, and both of them play an important role in conidiation and virulence in F. graminearum. We found that FgNTH resided in the cytoplasm, affected the localization of FgATH, and positively regulated DON biosynthesis; however, FgATH resided in vacuole and negatively regulated DON biosynthesis. FgNTH interacted with FgPK (pyruvate kinase), a key enzyme in glycolysis, and the interaction was reduced by VMA; the deficiency of FgNTH affected the localization of FgPK under DON induction condition. Strains with a deficiency of FgNTH were more sensitive to demethylation inhibitor (DMI) fungicides. FgNTH regulated the expression level of FgCYP51A and FgCYP51B by interacting with FgCYP51B. Taken together, VMA inhibits DON biosynthesis by targeting FgNTH and reducing the interaction between FgNTH and FgPK, and synergizes with DMI fungicides against F. graminearum by decreasing FgCYP51A and FgCYP51B expression.
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