Aflatoxin contamination in food and feed products has been brought into sharp focus over the last few decades in the world. However, there is no effective strategy for solving the problem thus far. Therefore, basic research on the aflatoxin-producer Aspergillus flavus is an urgent need. The vital role of mitogen-activated protein kinases (MAPKs) in signal transduction has been documented in various pathogenic fungi, but their functions in A. flavus have rarely been investigated. Herein, we characterized the detailed function of one of these MAPKs, AflSlt2. Targeted deletion of AflSlt2 gene indicates that this kinase is required for vegetative growth, conidia generation, and sclerotium formation. The analysis of AflSlt2 deletion mutant revealed hypersensitivity to cell wall-damaging chemicals and resistance against hydrogen peroxide. Interestingly, the ability of the ΔAflSlt2 mutant to generate aflatoxins in medium was significantly increased compared to wild type. However, a pathogenicity assay indicated that the ΔAflSlt2 mutant was deficient in peanut infection. Site-directed mutation study uncovered that the function of AflSlt2 was dependent on the phosphorylated residues (Thr-186 and Tyr-188) within the activation loop and the phosphotransfer residue (Lys-52) within the subdomain II. Interestingly, an autophosphorylation mutant of AflSlt2 (AflSlt2R66S) displayed wild type-like phenotypes. Bringing these observations together, we propose that Slt2-MAPK pathway is involved in development, stress response, aflatoxin biosynthesis, and pathogenicity in A. flavus. This study may be useful to unveil the regulation mechanism of aflatoxin biosynthesis and provide strategy to control A. flavus contamination.

中文翻译：

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MAP激酶AflSlt2调节黄曲霉真菌中黄曲霉毒素的生物合成和花生感染。

在过去的几十年中，食品和饲料产品中的黄曲霉毒素污染已成为人们关注的焦点。但是，到目前为止，还没有解决该问题的有效策略。因此，迫切需要对黄曲霉毒素生产者黄曲霉的基础研究。在各种致病真菌中均已证明了促分裂原活化蛋白激酶（MAPK）在信号转导中的重要作用，但很少研究它们在黄曲霉中的功能。在这里，我们表征了这些MAPK之一，AflSlt2的详细功能。AflSlt2基因的靶向缺失表明该激酶是营养生长，分生孢子生成和菌核形成所必需的。AflSlt2缺失突变体的分析显示对细胞壁破坏性化学物质超敏，对过氧化氢具有抗性。有趣的是 与野生型相比，ΔAflSlt2突变体在培养基中产生黄曲霉毒素的能力显着提高。但是，致病性分析表明，ΔAflSlt2突变体缺乏花生感染。定点突变研究发现，AflSlt2的功能取决于激活环内的磷酸化残基（Thr-186和Tyr-188）和亚结构域II内的磷酸转移残基（Lys-52）。有趣的是，AflSlt2（AflSlt2R66S）的自磷酸化突变体显示出类似野生型的表型。综合这些观察结果，我们建议Slt2-MAPK通路参与黄曲霉的发育，应激反应，黄曲霉毒素的生物合成和致病性。这项研究可能有助于揭示黄曲霉毒素生物合成的调控机制，并提供控制A的策略。