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

AaMYB15, an R2R3-MYB TF in Artemisia annua, acts as a negative regulator of artemisinin biosynthesis.
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AaMYB15 是青蒿中的 R2R3-MYB TF,作为青蒿素生物合成的负调节因子

DOI:
10.1016/j.plantsci.2021.110920
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发表时间:
2021-07
期刊:
Plant science : an international journal of experimental plant biology
影响因子:
--
通讯作者:
Tang K
Tang K
中科院分区:
其他
文献类型:
--
作者:
Wu Z;Li L;Liu H;Yan X;Ma Y;Li Y;Chen T;Wang C;Xie L;Hao X;Kayani SL;Tang K

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AaMYB 15负调控青蒿素生物合成。AaMYB 15间接抑制ADS、CYP 71 AV 1、DBR 2和ALDH 1的启动子活性。AaMYB 15与proAaORA结合并抑制其活性,从而下调下游关键酶基因。AaMYB 15响应于黑暗和JA处理。青蒿素是从黄花蒿中提取的一种次生代谢产物。青蒿素作为世界卫生组织认证的抗疟有效成分,具有广泛的经济价值。转录因子对青蒿素生物合成的正调节作用已被广泛研究,而负调节作用的研究却很少。在本研究中,我们鉴定了AaMYB 15作为第一个负调控青蒿素生物合成的R2 R3-MYB。annua。实验结果表明,AaMYB 15是一个核内转录因子,主要表达于A.青蒿素在annua合成和积累。黑暗和JA处理诱导AaMYB 15的表达。AaMYB 15的过表达导致关键酶基因ADS、ALDH 1、DBR 2和ALDH 1的表达水平显著下降,青蒿素含量显著降低。annua。AaMYB 15直接与JA信号通路中青蒿素生物合成的正调控因子AaORA的启动子结合,抑制其转录活性,从而下调下游关键酶基因的表达水平,负调控青蒿素的生物合成。本研究为A.一年生植物种质以及光和JA介导的青蒿素生物合成调控网络的新见解。
AaMYB15 negatively regulates artemisinin biosynthesis in Artemisia annua. AaMYB15 inhibits the promoter activities of ADS, CYP71AV1, DBR2, and ALDH1 indirectly. AaMYB15 binds to proAaORA and suppresses its activity, thus downregulating downstream key enzyme genes. AaMYB15 responds to dark and JA treatment. 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.
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