首页> 外文期刊>Scientific reports. >Whole-genome and time-course dual RNA-Seq analyses reveal chronic pathogenicity-related gene dynamics in the ginseng rusty root rot pathogen Ilyonectria robusta
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Whole-genome and time-course dual RNA-Seq analyses reveal chronic pathogenicity-related gene dynamics in the ginseng rusty root rot pathogen Ilyonectria robusta

机译:全基因组和时间课程双RNA-SEQ分析揭示人参生锈根腐毒素Ilyonectria Robusta中的慢性致病性相关基因动力学

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Ilyonectria robusta causes rusty root rot, the most devastating chronic disease of ginseng. Here, we for the first time report the high-quality genome of the I. robusta strain CD-56. Time-course (36?h, 72?h, and 144?h) dual RNA-Seq analysis of the infection process was performed, and many genes, including candidate effectors, were found to be associated with the progression and success of infection. The gene expression profile of CD-56 showed a trend of initial inhibition and then gradually returned to a profile similar to that of the control. Analyses of the gene expression patterns and functions of pathogenicity-related genes, especially candidate effector genes, indicated that the stress response changed to an adaptive response during the infection process. For ginseng, gene expression patterns were highly related to physiological conditions. Specifically, the results showed that ginseng defenses were activated by CD-56 infection and persisted for at least 144?h thereafter but that the mechanisms invoked were not effective in preventing CD-56 growth. Moreover, CD-56 did not appear to fully suppress plant defenses, even in late stages after infection. Our results provide new insight into the chronic pathogenesis of CD-56 and the comprehensive and complex inducible defense responses of ginseng root to I. robusta infection.
机译:Ilyonectria Robusta导致生锈的根腐,是人参最毁灭性的慢性病。在这里,我们首次报告I. Robusta菌株CD-56的高质量基因组。进行时间过程(36?H,72℃和144℃)对感染过程的双RNA-SEQ分析,并发现许多基因包括候选效果,包括感染的进展和成功相关。 CD-56的基因表达谱表现出初始抑制的趋势,然后逐渐返回到类似于控制的轮廓。分析基因表达模式和致病性相关基因的功能,尤其是候选效应基因,表明应力响应在感染过程中改变为适应性响应。对于人参,基因表达模式与生理条件高度相关。具体而言,结果表明,由CD-56感染激活人参防污,其后持续至少144℃,但调用的机制在预防CD-56的生长方面无效。此外,即使感染后的晚期阶段,CD-56也没有完全抑制植物防御。我们的结果为CD-56的慢性发病机制以及人参根对I. Robusta感染的综合性和复杂诱导防御反应提供了新的洞察力。

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