A Novel AP2/ERF Transcription Factor CR1 Regulates the Accumulation of Vindoline and Serpentine in Catharanthus roseus

As one type of the most important alkaloids in the world, terpenoid indole alkaloids (TIAs) show a wide range of pharmaceutical activities that are beneficial for clinical treatments. produces approximately 130 identified TIAs and is considered to be a model plant to study TIA biosynthesis. In order...

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Veröffentlicht in:Frontiers in plant science 2017-12, Vol.8, p.2082-2082
Hauptverfasser: Liu, Jiaqi, Gao, Fangyuan, Ren, Juansheng, Lu, Xianjun, Ren, Guangjun, Wang, Rui
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Sprache:eng
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Zusammenfassung:As one type of the most important alkaloids in the world, terpenoid indole alkaloids (TIAs) show a wide range of pharmaceutical activities that are beneficial for clinical treatments. produces approximately 130 identified TIAs and is considered to be a model plant to study TIA biosynthesis. In order to increase the production of high medical value metabolites whose yields are extremely low in , genetic engineering combined with transcriptional regulation has been applied in recent years. By using bioinformatics which is based on RNA sequencing (RNA-seq) data from methyl jasmonate (MeJA)-treated as well as phylogenetic analysis, the present work aims to screen candidate genes that may be involved in the regulation of TIA biosynthesis, resulting in a novel AP2/ERF transcription factor, CR1 (Catharanthus roseus 1). Subsequently, virus-induced gene silencing (VIGS) of was carried out to identify the involvement of CR1 in the accumulations of several TIAs and quantitative real-time PCR (qRT-PCR) was then applied to detect the expression levels of 7 genes in the related biosynthetic pathway in silenced plants. The results show that all the 7 genes were upregulated in -silenced plants. Furthermore, metabolite analyses indicate that silencing could increase the accumulations of vindoline and serpentine in . These results suggest a novel negative regulator which may be involved in the TIAs biosynthetic pathway.
ISSN:1664-462X
1664-462X
DOI:10.3389/fpls.2017.02082