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Transcriptional regulation of the porcine miR-17-92 cluster

文献类型： 外文期刊

作者： Yang, Xiu-qin 1 ; Zhang, Cai-xia 1 ; Wang, Jin-kui 1 ; Wang, Liang 2 ; Du, Xin 1 ; Song, Yan-fang 1 ; Liu, Di 2 ;

作者机构： 1.Northeast Agr Univ, Coll Anim Sci & Technol, Harbin, Heilongjiang, Peoples R China

2.Heilongjiang Acad Agr Sci, Inst Anim Husb, Harbin, Heilongjiang, Peoples R China

关键词： Pig; miR-17-92 cluster; Promoter; cis-regulatory element; Transcription factor

期刊名称：MOLECULAR GENETICS AND GENOMICS （ 影响因子：3.291； 五年影响因子：3.257 ）

ISSN： 1617-4615

年卷期： 2019 年 294 卷 4 期

页码：

收录情况： SCI

摘要： The miR-17-92 cluster has been involved in the cell cycle, apoptosis, and signaling. However, its transcriptional regulation has not been fully characterized. To elucidate the transcriptional regulation, the promoter of miR-17-92 was analyzed in detail in pig here. We found that, as an intronic miRNA, porcine miR-17-92 cluster was regulated by two independent promoters, an A/T-rich region directly upstream of the miR-17-92 coding sequence, and a G/C-rich region corresponding to the host gene promoter of the human miR-17-92 cluster. Several cis-regulatory elements were identified including sites for c-Myc, NFY, E2F3, and SP1, among which NFY and c-Myc sites were present in both A/T- and G/C-rich regions, while E2F3 and SP1 sites only existed in G/C-rich region. Sites for c-Myc, E2F3, and SP1 were positive for regulating transcription. NFY sites played bipartite roles, functioning as a repressor for the A/T-rich region, and as an activator for the G/C-rich region. Additionally, we found that levels of individual miRNAs in the cluster were not promoted completely in parallel with each other or with pri-miR-17-92 by the A/T-rich region, through using a self-made vector by modifying pGL3-basic in which firefly luciferase gene was replaced with an miR-17-92 cluster and a direct upstream A/T-rich region. The expression regulation of miR-17-92 is complicated and the results will contribute to further revealing the regulatory mechanisms under the expression of the miR-17-92 cluster.

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