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Effects of glucans and eicosapentaenoic acid on differential regulation of phenylpropanoid and mevalonic pathways during potato response to Phytophthora infestans

机译:葡聚糖和二十碳五烯酸对马铃薯对疫霉疫霉反应期间苯丙烷和甲羟戊酸途径差异调节的影响

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The effects of Phytophthora infestans glucans, eicosapentaenoic acid (EPA) and isolates of this pathogen, on the differential expression of eight genes from the phenylpropanoid and the mevalonate (Ac-MVA) pathways were analyzed in potato by semi-quantitative RT-PCR and qRT-PCR. The application of EPA had an elicitor effect in Russet Burbank (RB) and Defender (DF) in response to inoculation with a US8 isolate of P. infestans, thereby reducing symptoms of late blight. Such effect was associated with the expression of PAL-1 and PAL-2, since the latter occurred only when EPA was followed by inoculation, whereas these genes were down-regulated in individual treatments RB + EPA, RB + US8, DF + EPA, and DF + US8. The glucan fraction did not by itself suppress phenylpropanoid genes, but its combination with the pathogen resulted in a down-regulation of PAL-1, PAL-2 and CHS. The addition of the glucan fraction to the elicitor EPA, had a negative effect (RB + EPA + GL + US8) since plants showed higher disease symptoms than the ones pretreated with water then infected with US8, and in comparison with RB + EPA + US8 and RB + GL + US8. Exclusive up-regulation of 4CL in DF + US11 and of CHS in DF + EPA + GL + US8, DF + EPA + US11, DF + GL + US11 and DF + EPA + GL + US11, where late blight lesions were not detected, could be associated with potato protection against late blight. Along with previous findings in this pathosystem, these data suggest that genetic resistance in potato against P. infestans is not the result of isolated reactions against the pathogen, but rather the combination of many factors in-line with a polygenic/horizontal resistance.
机译:通过半定量RT-PCR和qRT分析了马铃薯疫霉菌葡聚糖,二十碳五烯酸(EPA)和该病原体的分离对苯基丙烷和甲羟戊酸(Ac-MVA)途径八个基因差异表达的影响-PCR。 EPA的应用对US8感染的P. infestans分离株有反应,对Russet Burbank(RB)和Defender(DF)具有激发作用,从而减轻了晚疫病的症状。这种作用与PAL-1和PAL-2的表达有关,因为后者仅在接种EPA之后才发生,而这些基因在单独的处理RB + EPA,RB + US8,DF + EPA,和DF + US8。葡聚糖部分本身并不能抑制苯基丙烷基因,但其与病原体的结合导致PAL-1,PAL-2和CHS的下调。将葡聚糖级分添加到引发剂EPA中具有负面影响(RB + EPA + GL + US8),因为植物显示出的病害症状高于用水预处理后再感染US8的植物,并且与RB + EPA + US8相比和RB + GL + US8。 DF + US11中的4CL和DF + EPA + GL + US8,DF + EPA + US11,DF + GL + US11和DF + EPA + GL + US11的CHS独家上调,其中未检出晚疫病灶,可能与马铃薯防晚疫病有关。连同该病理系统中的先前发现,这些数据表明马铃薯对致病疫霉的遗传抗性不是针对病原体的孤立反应的结果,而是许多因素与多基因/水平抗性一致的组合。

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