Penicillium expansum, as the causal agent of blue mould and a main producer of mycotoxin patulin, is a global concern for economic and food safety. To date, the nutritional requirements of the pathogen during infection and patulin biosynthesis are poorly understood. Here, we genetically characterized the role of the bZIP transcription factor PeMetR in sulfur metabolism, virulence and patulin biosynthesis of P. expansum. The PeMetR regulator is crucial for normal germination and growth on inorganic S-sources but dispensable for utilization of organic S-sources. Accordingly, it is involved in regulating the expression of genes in sulfur assimilation pathway rather than methionine metabolic processes. Disruption of PeMetR resulted in a complete loss of virulence on various fruits. Additionally, the mutant showed a remarkably reduced ability to produce patulin. Exogenous methionine could partially or completely rescue the impaired phenotypes of the mutant. Inactivation of the sulfur assimilation pathway genes, PesA, PesB, PesC, PesF, generated growth, virulence and patulin production defects similar to those of ΔPeMetR. Overall, our study provides evidence that PeMetR-mediated sulfur assimilation is essential for growth and infection and shows for the first time that regulation of sulfur assimilation affects biosynthesis of an important mycotoxin patulin in P. expansum.

中文翻译：

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PeMetR 介导的硫同化对于膨胀青霉的毒力和展青霉素生物合成至关重要

Penicillium expansum作为蓝霉病的病原体和展曲霉素的主要生产者，是全球经济和食品安全问题。迄今为止，对病原体在感染和展青霉素生物合成过程中的营养需求知之甚少。在这里，我们对 bZIP 转录因子 PeMetR 在P. expansum 的硫代谢、毒力和展青霉素生物合成中的作用进行了遗传表征。PeMetR 调节器对于无机 S 源的正常发芽和生长至关重要，但对于有机 S 源的利用却是可有可无的。因此，它参与调节硫同化途径而非蛋氨酸代谢过程中基因的表达。PeMetR 的中断导致对各种水果的毒力完全丧失。此外，该突变体显示出产生展青霉素的能力显着降低。外源蛋氨酸可以部分或完全挽救突变体受损的表型。硫同化途径基因PesA、PesB、PesC、PesF 的失活产生类似于 Δ PeMetR 的生长、毒力和展青霉素生产缺陷。总体而言，我们的研究提供了证据，证明 PeMetR 介导的硫同化对于生长和感染至关重要，并首次表明硫同化的调节影响P. expansum 中重要的霉菌毒素展青霉素的生物合成。