Time-Course Transcriptome Analysis Reveals Resistance Genes of Panax ginseng Induced by Cylindrocarpon destructans Infection Using RNA-Seq

نویسندگان

  • Yuan Gao
  • Xiaoli He
  • Bin Wu
  • Qiliang Long
  • Tianwei Shao
  • Zi Wang
  • Jianhe Wei
  • Yong Li
  • Wanlong Ding
  • Shilin Chen
چکیده

Panax ginseng C. A. Meyer is a highly valued medicinal plant. Cylindrocarpon destructans is a destructive pathogen that causes root rot and significantly reduces the quality and yield of P. ginseng. However, an efficient method to control root rot remains unavailable because of insufficient understanding of the molecular mechanism underlying C. destructans-P. ginseng interaction. In this study, C. destructans-induced transcriptomes at different time points were investigated using RNA sequencing (RNA-Seq). De novo assembly produced 73,335 unigenes for the P. ginseng transcriptome after C. destructans infection, in which 3,839 unigenes were up-regulated. Notably, the abundance of the up-regulated unigenes sharply increased at 0.5 d postinoculation to provide effector-triggered immunity. In total, 24 of 26 randomly selected unigenes can be validated using quantitative reverse transcription (qRT)-PCR. Gene ontology enrichment analysis of these unigenes showed that "defense response to fungus", "defense response" and "response to stress" were enriched. In addition, differentially expressed transcription factors involved in the hormone signaling pathways after C. destructans infection were identified. Finally, differentially expressed unigenes involved in reactive oxygen species and ginsenoside biosynthetic pathway during C. destructans infection were indentified. To our knowledge, this study is the first to report on the dynamic transcriptome triggered by C. destructans. These results improve our understanding of disease resistance in P. ginseng and provide a useful resource for quick detection of induced markers in P. ginseng before the comprehensive outbreak of this disease caused by C. destructans.

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عنوان ژورنال:

دوره 11  شماره 

صفحات  -

تاریخ انتشار 2016