Abstract
Artemisia annua L. is known for its specific product “artemisinin” which is an active ingredient for curing malaria. Artemisinin is secreted and accumulated in the glandular secretory trichomes (GSTs) on A. annua leaves. Earlier studies have shown that increasing GST density is effective in increasing artemisinin content. However, the mechanism of GST initiation is not fully understood. To this end, we isolated and characterized an R2R3-MYB gene, AaMYB17, which is expressed specifically in the GSTs of shoot tips. Overexpression of AaMYB17 in A. annua increased GST density and enhanced the artemisinin content, whereas RNA interference of AaMYB17 resulted in the reduction of GST density and artemisinin content. Additionally, neither overexpression lines nor RNAi lines showed an abnormal phenotype in plant growth and the morphology of GSTs. Our study demonstrates that AaMYB17 is a positive regulator of GSTs’ initiation, without influencing the trichome morphology.
Highlights
Malaria is a mosquito-borne infectious disease caused by the Plasmodium species which targets human red blood cells (Wilson et al, 2011)
The characteristic of “HMAQWESARxEAEAxLxMDS” demonstrated that contig133232 belonged to subgroup 9 of R2R3-MYBs (Stracke et al, 2001; Brockington et al, 2013)
Former studies revealed that MIXTA/MIXTA-like TFs play an important role in the regulation of trichome initiation or cell development
Summary
Malaria is a mosquito-borne infectious disease caused by the Plasmodium species which targets human red blood cells (Wilson et al, 2011). Artemisinin-based combination therapy (ACT) is considered the most efficient treatment to cure malaria (World Health Organization [WHO], 2019). Artemisinin is a bioactive compound, synthesized and accumulated in the glandular trichome of a traditional Chinese herb, Artemisia annua L. Trichomes are unicellular or multicellular structures derived from aerial epidermal cells (Duke and Paul, 2013). Their morphological diversity, different number of cells, and their potential in secondary metabolism distinguish them from each other (Werker, 2000; Serna and Martin, 2006).
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