Functional genomics-guided discovery of a light-activated phytotoxin in the wheat pathogen Parastagonospora nodorum via pathway activation

Functional genomics-guided discovery of a light-activated phytotoxin in the wheat pathogen Parastagonospora nodorum via pathway activation
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DOI:
10.1111/1462-2920.13711
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发表时间:
2017-05-01
影响因子:
5.1
通讯作者:
Solomon, Peter S.
Solomon, Peter S.
中科院分区:
生物学2区
文献类型:
--
作者:
Chooi, Yit-Heng;Zhang, Guozhi;Solomon, Peter S.

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小麦颖枯病是小麦的重要病原菌。次级代谢产物对这一病理系统的贡献知之甚少。已经显示生物合成基因簇(SNOG_08608-08616)在颖枯病菌小麦叶感染的后期阶段被上调。该基因簇与编码尾孢菌素生物合成的烟草尾孢菌CTB基因簇共享几个同源物。通过过表达(OE)颖枯菌中的转录因子基因(SNOG_08609)激活基因簇导致产生痂囊腔菌素C,一种结构上类似于尾孢菌素的perelyenequinone植物毒素。来自构巢曲霉中基因簇的聚酮合酶基因elcA的异源表达导致尾孢菌素途径中常见的聚酮前体去甲内酯的产生。痂囊腔菌素C可以在感染颖枯病菌的小麦叶片中检测到,但在elcA破坏突变体中检测不到。该化合物显示出以光依赖性方式对小麦叶片表现出坏死活性。小麦幼苗感染试验表明,elcA表现出降低的毒力与野生型相比,而感染的OE菌株过量生产痂囊腔菌素C导致叶片上的较大病变。这些数据提供了证据,痂囊腔菌素C有助于对小麦的致病性的P. nodorum。
Parastagonospora nodorum is an important pathogen of wheat. The contribution of secondary metabolites to this pathosystem is poorly understood. A biosynthetic gene cluster (SNOG_08608-08616) has been shown to be upregulated during the late stage of P. nodorum wheat leaf infection. The gene cluster shares several homologues with the Cercospora nicotianae CTB gene cluster encoding the biosynthesis of cercosporin. Activation of the gene cluster by overexpression (OE) of the transcription factor gene (SNOG_08609) in P. nodorum resulted in the production of elsinochrome C, a perelyenequinone phytotoxin structurally similar to cercosporin. Heterologous expression of the polyketide synthase gene elcA from the gene cluster in Aspergillus nidulans resulted in the production of the polyketide precursor nortoralactone common to the cercosporin pathway. Elsinochrome C could be detected on wheat leaves infected with P. nodorum, but not in the elcA disruption mutant. The compound was shown to exhibit necrotic activity on wheat leaves in a light-dependent manner. Wheat seedling infection assays showed that elcA exhibited reduced virulence compared with wild type, while infection by an OE strain overproducing elsinochrome C resulted in larger lesions on leaves. These data provided evidence that elsinochrome C contributes to the virulence of P. nodorum against wheat.