The roles of AaMIXTA1 in regulating the initiation of glandular trichomes and cuticle biosynthesis in Artemisia annua.
Pu ShiXueqing FuQian ShenMeng LiuQifang PanYueli TangWeimin JiangZongyou LvTingxiang YanYanan MaMinghui ChenXiaolong HaoPin LiuLing LiXiaofen SunKexuan TangPublished in: The New phytologist (2017)
The glandular secretory trichomes (GSTs) on Artemisia annua leaves have the capacity to secrete and store artemisinin, a compound which is the most effective treatment for uncomplicated malaria. An effective strategy to improve artemisinin content is therefore to increase the density of GSTs in A. annua. However, the formation mechanism of GSTs remains poorly understood. To explore the mechanisms of GST initiation in A. annua, we screened myeloblastosis (MYB) transcription factor genes from a GST transcriptome database and identified a MIXTA transcription factor, AaMIXTA1, which is expressed predominantly in the basal cells of GST in A. annua. Overexpression and repression of AaMIXTA1 resulted in an increase and decrease, respectively, in the number of GSTs as well as the artemisinin content in transgenic plants. Transcriptome analysis and cuticular lipid profiling showed that AaMIXTA1 is likely to be responsible for activating cuticle biosynthesis. In addition, dual-luciferase reporter assays further demonstrated that AaMIXTA1 could directly activate the expression of genes related to cuticle biosynthesis. Taken together, AaMIXTA1 regulated cuticle biosynthesis and prompted GST initiation without any abnormal impact on the morphological structure of the GSTs and so provides a new way to improve artemisinin content in this important medicinal plant.
Keyphrases
- transcription factor
- plasmodium falciparum
- genome wide identification
- cell wall
- genome wide
- dna binding
- induced apoptosis
- single cell
- poor prognosis
- gene expression
- dna methylation
- bioinformatics analysis
- high throughput
- signaling pathway
- crispr cas
- rna seq
- cell proliferation
- endoplasmic reticulum stress
- fatty acid
- cell death
- drug induced
- genome wide analysis
- adverse drug
- replacement therapy
- smoking cessation