Comparison of miRNA-101a-3p and miRNA-144a-3p regulation with the key genes of alpaca melanocyte pigmentation

IF 2.946 Q3 Biochemistry, Genetics and Molecular Biology

BMC Molecular Biology Pub Date : 2019-08-14 DOI:10.1186/s12867-019-0137-8

Zhiwei Zhu, Yueyue Ma, Yuan Li, Zhixue Cheng, Huifeng Li, Lihuan Zhang, Dongmei Xu, Pengfei Li

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引用次数: 2

Abstract

Many miRNA functions have been revealed to date. Single miRNAs can participate in life processes by regulating more than one target gene, and more than one miRNA can also simultaneously act on one target mRNA. Thus, a complex regulatory network involved in many processes can be formed. Herein, the pigmentation regulation mechanism of miR-101a-3p and miR-144a-3p was studied at the cellular level by the overexpression and equal overexpression of miR-101a-3p and miR-144a-3p.

Results revealed that miR-101a-3p and miR-144a-3p directly regulated the expression of microphthalmia-associated transcription factor, thereby affecting melanin synthesis.

The two miRNAs with the same binding site in the same gene independently excreted each other’s function. However, the inhibitory effect of miR-144a-3p was stronger than that of miR-101-3p in alpaca melanocytes, although both decreased melanin production.

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miRNA-101a-3p和miRNA-144a-3p调控羊驼黑素细胞色素沉着关键基因的比较

迄今为止，已经发现了许多miRNA的功能。单个miRNA可以通过调控多个靶基因参与生命过程，多个miRNA也可以同时作用于一个靶mRNA。因此，可以形成一个涉及许多过程的复杂调节网络。本文通过对miR-101a-3p和miR-144a-3p的过表达和等过表达，在细胞水平上研究miR-101a-3p和miR-144a-3p的色素沉着调节机制。结果显示，miR-101a-3p和miR-144a-3p可直接调控小眼相关转录因子的表达，从而影响黑色素的合成。在同一基因中具有相同结合位点的两个mirna各自独立地排泄彼此的功能。然而，miR-144a-3p在羊驼黑素细胞中的抑制作用强于miR-101-3p，尽管两者都降低了黑色素的产生。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

BMC Molecular Biology 生物-生化与分子生物学

CiteScore

4.80

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： BMC Molecular Biology is an open access journal publishing original peer-reviewed research articles in all aspects of DNA and RNA in a cellular context, encompassing investigations of chromatin, replication, recombination, mutation, repair, transcription, translation and RNA processing and function.