MicroRNA-184 downregulates nuclear receptor corepressor 2 in mouse spermatogenesis

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.MiR-184 may be involved in the post-transcription regulation of mRNAs such as Ncor2 in mammalian spermatogenesis.Spermatogenesis is a highly regulated process of germ cell differentiation that can be subdivided into three main phases: spermatogonial proliferation, meiosis of spermatocytes and spermiogenesis of haploid spermatids. The meiotic and haploid phases of spermatogenesis are characterized by high transcriptional activity but suppressed translational activity. Post-transcriptional control of gene expression in these phases is a significant feature of mammalian spermatogenesis [1]. MicroRNAs (miRNAs) are a family of small non-coding RNAs (typically 19~23 nt), which play important roles in regulating post-transcriptional gene silence through base-pair binding to their target mRNA [2]. Emerging evidences have suggested that the involvement of miRNAs in mammalian spermatogenesis. First, numerous miRNAs are exclusively or preferentially expressed in the mouse testis [3]. Second, the pattern of miRNA expression appears to be different between immature and mature mouse testis [4]. Last but not least, spermatogenesis is disrupted at the early stage of proliferation and/or early differentiation in mouse in which the Dicer gene, encoding an RNase III required for miRNA processing, has been deleted in the testis [5]. Additionally, several studies have indicated that some miRNAs participate in mammalian spermatogenesis. For example, miRNA-122a reduces the expression of the post-transcriptionally regulated germ cell transition