AaMYB108 is the core factor integrating light and jasmonic acid signaling to regulate artemisinin biosynthesis in Artemisia annua.

Artemisinin, a sesquiterpene compound synthesized and stored in the glandular trichome of Artemisia annua leaves, has been used to treat malaria. Previous studies have shown that both light and jasmonic acid (JA) can promote the biosynthesis of artemisinin, and the promotion of artemisinin by JA is dependent on light. However, the specific molecular mechanism remains unclear. Here, we report a MYB transcription factor, AaMYB108, identified from transcriptome analysis of light and JA treatment, as a positive regulator of artemisinin biosynthesis in A. annua. AaMYB108 promotes artemisinin biosynthesis by interacting with a previously characterized positive regulator of artemisinin, AaGSW1. Then, we found that AaMYB108 interacted with AaCOP1 and AaJAZ8, respectively. The function of AaMYB108 was influenced by AaCOP1 and AaJAZ8. Through the treatment of AaMYB108 transgenic plants with light and JA, it was found that the promotion of artemisinin by light and JA depends on the presence of AaMYB108. Taken together, our results reveal the molecular mechanism of JA regulating artemisinin biosynthesis depending on light in A. annua. This study provides new insights into the integration of light and phytohormone signaling to regulate terpene biosynthesis in plants.

The WRKY transcription factor AaGSW2 promotes glandular trichome initiation in Artemisia annua.

Glandular secreting trichomes (GSTs) synthesize and secrete large quantities of secondary metabolites, some of which have well-established commercial value. An example is the anti-malarial compound artemisinin, which is synthesized in the GSTs of Artemisia annua. Accordingly, there is considerable interest in understanding the processes that regulate GST density as a strategy to increase artemisinin production. In this study, we identified a GST-specific WRKY transcription factor from A. annua, AaGSW2, which is positively regulated by the direct binding of the homeodomain proteins AaHD1 and AaHD8 to the L1-box of the AaGSW2 promoter. Overexpression of AaGSW2 in A. annua significantly increased GST density, while AaGSW2 knockdown lines showed impaired GST initiation. Ectopic expression of AaGSW2 homologs from two mint cultivars, Mentha spicata and Mentha haplocalyx, in A. annua also induced GST formation. These results reveal a molecular mechanism involving homeodomain and WRKY proteins that controls glandular trichome initiation, at least part of which is shared by A. annua and mint.

AaMYB15, an R2R3-MYB TF in Artemisia annua, acts as a negative regulator of artemisinin biosynthesis.

Artemisinin is a secondary metabolite extracted from Artemisia annua. As an effective antimalarial component certified by WHO, artemisinin has extensive economical values. Numerous studies about transcription factors positively regulating artemisinin biosynthesis have been published while negative regulators are rarely reported. In the present study, we identified AaMYB15 as the first R2R3-MYB that negatively regulates artemisinin biosynthesis in A. annua. Experimental evidences showed that AaMYB15 is a transcription factor within nucleus and predominantly expressed in glandular secretory trichomes (GSTs) in A. annua where artemisinin is synthesized and accumulated. The expression of AaMYB15 was induced by dark and JA treatment. Overexpression of AaMYB15 led to a significant decline in the expression levels of key enzyme genes ADS, CYP, DBR2, and ALDH1 and a significant decrease in the artemisinin contents of transgenic A. annua. AaMYB15 directly bound to the promoter of AaORA, a reported positive regulator of artemisinin biosynthesis in JA signaling pathway, to repress its transcriptional activity, thus downregulating the expression levels of downstream key enzyme genes and negatively regulating the artemisinin biosynthesis. Our study provides candidate gene for improvement of A. annua germplasm and new insights into the artemisinin biosynthesis regulation network mediated by light and JA.