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微小RNA-184在小鼠精子发生过程中下调核受体辅阻遏物2

MicroRNA-184 downregulates nuclear receptor corepressor 2 in mouse spermatogenesis.

作者信息

Wu Jingwen, Bao Jianqiang, Wang Li, Hu Yanqin, Xu Chen

机构信息

Department of Histology & Embryology, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.

出版信息

BMC Dev Biol. 2011 Oct 24;11:64. doi: 10.1186/1471-213X-11-64.

DOI:10.1186/1471-213X-11-64
PMID:22017809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3227627/
Abstract

BACKGROUND

There have been increasing attentions on the role of small RNAs, especially microRNAs in post-transcriptional gene regulation during spermatogenesis. MicroRNA-184 (miR-184) has been shown to be mainly expressed in the testis and brain, and that its expression levels are by far the highest in the testis. However, the role of miR-184 in mammalian spermatogenesis remains unclear.

RESULTS

In this study, we demonstrated that miR-184 levels were increased during mouse postnatal testis development. Specifically, miR-184 expression was restricted to the germ cells from spermatogonia to round spermatids. Overexpression of miR-184 promoted the proliferation of a germ cell line, GC-1spg. Moreover, miR-184 downregulated nuclear receptor corepressor 2 (Ncor2) by targeting its 3' untranslated region through inhibiting NCOR2 protein translation.

CONCLUSIONS

MiR-184 may be involved in the post-transcription regulation of mRNAs such as Ncor2 in mammalian spermatogenesis.

摘要

背景

小RNA,尤其是微小RNA在精子发生过程中的转录后基因调控作用受到越来越多的关注。微小RNA - 184(miR - 184)已被证明主要在睾丸和大脑中表达,且其在睾丸中的表达水平目前是最高的。然而,miR - 184在哺乳动物精子发生中的作用仍不清楚。

结果

在本研究中,我们证明了miR - 184水平在小鼠出生后睾丸发育过程中升高。具体而言,miR - 184的表达局限于从精原细胞到圆形精子细胞的生殖细胞。miR - 184的过表达促进了生殖细胞系GC - 1spg的增殖。此外,miR - 184通过靶向核受体辅阻遏物2(Ncor2)的3'非翻译区,抑制NCOR2蛋白翻译,从而下调Ncor2。

结论

MiR - 184可能参与哺乳动物精子发生过程中如Ncor2等mRNA的转录后调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/fcb40f038e6d/1471-213X-11-64-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/c57636ebd22f/1471-213X-11-64-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/e6e86f7cbded/1471-213X-11-64-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/c083422e8843/1471-213X-11-64-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/2f91c6cc433d/1471-213X-11-64-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/fcb40f038e6d/1471-213X-11-64-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/c57636ebd22f/1471-213X-11-64-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/e6e86f7cbded/1471-213X-11-64-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/c083422e8843/1471-213X-11-64-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/2f91c6cc433d/1471-213X-11-64-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db6/3227627/fcb40f038e6d/1471-213X-11-64-5.jpg

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