The pH-responsive PacC transcription factor plays pivotal roles in virulence and patulin biosynthesis in Penicillium expansum
The pH-responsive PacC transcription factor plays pivotal roles in virulence and patulin biosynthesis in Penicillium expansum
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pH 响应性 PacC 转录因子在扩展青霉的毒力和展青霉素生物合成中发挥关键作用
DOI：
10.1111/1462-2920.14453
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发表时间：
2018-11-01
影响因子：
5.1
通讯作者：
Tian, Shiping
中科院分区：
文献类型：
--
作者：
Chen, Yong;Li, Boqiang;Tian, Shiping
PacC（磷酸酶活性在酸性而非碱性条件下的丧失或降低[Pac]）转录因子调节许多真菌病原体的环境适应、次生代谢和毒力。本文报道了PacC在园艺作物采后病原菌——绿青霉（Penicillium expansum）中的功能，并确定了PePacC的基因表达和蛋白水解过程严格依赖于ph值。在酸性和碱性条件下，PePacC的缺失均导致白皮的生长和分生能力明显下降。在pH值高于6.0时，Delta PePacC突变体失去了产生棒曲霉素的能力，因为棒曲霉素簇中所有基因的表达均显著下调。此外，δ PePacC突变体在梨和苹果果实中的毒力明显降低。蛋白质组学分析表明，PePacC可作为钙网蛋白（PeCRT）和硫酸腺苷基转移酶（PeSAT）等不同靶蛋白的激活或抑制蛋白，进一步证实了这些靶蛋白参与了芽孢杆菌的毒力。我们的研究结果表明，PePacC通过限制簇中基因的表达，在展霉素生物合成中发挥重要作用，并通过介导已知的毒力因子葡萄糖氧化酶（PeGOD）和新的毒力因子，如PeCRT和PeSAT，在发病机制中发挥重要作用。
The PacC (loss or reduction in phosphatase activity at acid but not at alkaline pH [Pac]) transcription factor regulates environmental adaptation, secondary metabolism and virulence in many fungal pathogens. Here, we report the functions of PacC in Penicillium expansum, a postharvest pathogenic fungus in horticultural crops, and ascertain that the gene expression and proteolytic processing of PePacC are strictly pH-dependent. Loss of PePacC resulted in an obvious decrease in growth and conidiation of P. expansum cultured in both acidic and alkaline conditions. The Delta PePacC mutant lost the ability of patulin production at pH values above 6.0 because expressions of all the genes in patulin cluster were significantly down-regulated. Additionally, virulence of the Delta PePacC mutant was obviously reduced in pear and apple fruits. Proteome analysis revealed that PePacC could function as an activator or repressor for different target proteins, including calreticulin (PeCRT) and sulfate adenylyltransferase (PeSAT), which were further proved to be involved in virulence of P. expansum. Our results demonstrate important roles for PePacC in patulin biosynthesis via limiting expressions of the genes in the cluster, and in pathogenesis via mediating a known virulence factor glucose oxidase (PeGOD) and new virulence factors, such as PeCRT and PeSAT.