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首页> 外文期刊>Journal of Ginseng Research >Transcriptome analyses of the ginseng root rot pathogens Cylindrocarpon destructans and Fusarium solani to identify radicicol resistance mechanisms
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Transcriptome analyses of the ginseng root rot pathogens Cylindrocarpon destructans and Fusarium solani to identify radicicol resistance mechanisms

机译:人参根腐病病原体曲圆柱损伤的转录组分析和镰刀菌索兰尼鉴定基因硅抗性机制

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Background The ascomycete fungi Cylindrocarpon destructans (Cd) and Fusarium solani (Fs) cause ginseng root rot and significantly reduce the quality and yield of ginseng. Cd produces the secondary metabolite radicicol, which targets the molecular chaperone Hsp90. Fs is resistant to radicicol, whereas other fungal genera associated with ginseng disease are sensitive to it. Radicicol resistance mechanisms have not yet been elucidated. Methods Transcriptome analyses of Fs and Cd mycelia treated with or without radicicol were conducted using RNA-seq. All of the differentially expressed genes (DEGs) were functionally annotated using the Fusarium graminearum transcript database. In addition, deletions of two transporter genes identified by RNA-seq were created to confirm their contributions to radicicol resistance. Results Treatment with radicicol resulted in upregulation of chitin synthase and cell wall integrity genes in Fs and upregulation of nicotinamide adenine dinucleotide dehydrogenase and sugar transporter genes in Cd. Genes encoding an ATP-binding cassette transporter, an aflatoxin efflux pump, ammonium permease 1 ( mep1 ), and nitrilase were differentially expressed in both Fs and Cd. Among these four genes, only the ABC transporter was upregulated in both Fs and Cd. The aflatoxin efflux pump and mep1 were upregulated in Cd, but downregulated in Fs, whereas nitrilase was downregulated in both Fs and Cd. Conclusion The transcriptome analyses suggested radicicol resistance pathways, and deletions of the transporter genes indicated that they contribute to radicicol resistance.
机译:背景技术Ascomycete真菌Cylindrocarpon Destructans(CD)和镰刀菌(FS)导致人参根腐烂,显着降低人参的质量和产量。 CD产生次级代谢物加基因硅,其靶向分子伴侣Hsp90。 FS对拉基硅耐药,而与人参疾病相关的其他真菌属对其敏感。尚未阐明基霉素抗性机制。方法使用RNA-SEQ进行有或不含无基理治疗FS和CD菌丝体的转录组分析。所有差异表达的基因(DEGS)都是使用镰刀·克柳素转录物数据库在功能上注释的。此外,产生由RNA-SEQ鉴定的两种转运基因的缺失,以证实它们对抗性的抗性抗性的贡献。基于CD中的CD和甘氨酸腺嘌呤二核苷酸脱氢酶和甘油转运蛋白基因的FS和Uproputation in Chitin合酶和细胞壁完整性脱氢酶和糖转运蛋白基因的丁蛋白合成酶和细胞壁完整性基因的上调。编码ATP结合盒式磁带转运盒的基因,在FS和CD中差异表达了氧化术杂交泵,铵氧化酶输出泵,溶液允许1(MEP1)和腈酶。在这四种基因中,仅在FS和Cd中仅令止血剂。在CD中升高了黄曲霉毒素渗透泵和MEP1,但在FS中下调,而硝基菌酶在FS和CD中下调。结论转录组分析提出了基因菌抵抗途径,并缺失转运蛋白基因表明它们有助于抗性硅。

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