Abstract

Previous studies indicated that miR-29c is important for muscle development in mice and human, but its role in pigs is unknown. In this study, we detected the expression of miR-29c in Meishan longissimus lumborum (LL) muscle. The results showed that miR-29c was gradually upregulated during development of skeletal muscle in pig. Moreover, the expression of YY1 and Akt3 genes, which were confirmed to be targeted by miR-29c in mice, was decreased along with muscle development. Furthermore, the expression level of miR-29c was significantly higher in adult Meishan pigs than Large White pigs, while the expression of YY1 and Akt3 genes was significantly lower in Meishan pigs. These results indicated that the expression pattern of miR-29c was opposite to that of YY1 and Akt3 genes in pigs. Also, the luciferase assay indicated that miR-29s can target the YY1 gene in pigs. In addition, we identified a T to C mutation in the primary transcript of miR-29c, which was associated with the postmortem muscle pH in pigs. Based on these results, we concluded that miR-29c is also important in skeletal muscle development of pigs.

Highlights

  • MicroRNAs are a class of small non-coding RNAs[1,2] can inhibit target genes through binding with their 3′ untranslated regions (3′ UTR)[3]

  • To test whether the YY1 gene was targeted by miR-29c in pigs, the conservation of target site of the miR-29c in the YY1 gene was analyzed

  • The results showed that miR-29a, miR-29b and miR-29c could significantly inhibit the luciferase activity when the 3′ UTR was inserted (Fig. 1b)

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Summary

Introduction

MicroRNAs are a class of small non-coding RNAs[1,2] can inhibit target genes through binding with their 3′ untranslated regions (3′ UTR)[3]. Previous studies showed that microRNAs can participate in cell proliferation, differentiation and apoptosis[4,5,6]. MiR-29 can participate in many physiological and chemical processes. It has been reported that miR29a can inhibit apoptosis and protect the mitochondrial functions during forebrain ischemia through targeting the pro-apoptosis PUMA gene in astrocytes[8]. Many studies have shown that miR-29s can inhibit tissue fibrosis through downregulating collagen genes and inhibition of IGF-1 and PDGC growth factors[5,9,10]. MiR29s can restrain the activities of DNA methyltransferases and demethylases[11], promote murine osteoclastogenesis[12] and inhibit tumorigenesis[13]

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