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The elaborate interplay of coding and noncoding factors governs muscle growth and development. Here, we reported a mutual activation between long noncoding RNA (lncRNA) H19 and MyoD (myogenic determination gene number 1) in the muscle process. We successfully cloned the two isoforms of goat H19, which were significantly enriched and positively correlated with MyoD transcripts in skeletal muscles or differentiating muscle satellite cells (MuSCs). To systematically screen genes altered by H19, we performed RNA-seq using cDNA libraries of differentiating H19-deficiency MuSCs and consequently anchored MyoD as the critical genes in mediating H19 function. Intriguingly, some transcripts of MyoD and H19 overlapped in the cytoplasm, which was dramatically damaged when the core complementary nucleotides were mutated. Meanwhile, MyoD RNA successfully pulled down H19 in MS2-RIP experiments. Furthermore, HuR could bind both H19 and MyoD transcripts, while H19 or its truncated mutants successfully stabilized MyoD mRNA, with or without HuR deficiency. In turn, novel functional MyoD protein-binding sites were identified in the promoter and exons of the H19 gene. Our results suggest that MyoD activates H19 transcriptionally, and RNA-RNA hybridization is critical for H19-promoted MyoD expression, which extends our knowledge of the hierarchy of regulatory networks in muscle growth. • H19 promotes differentiation of goat skeletal muscle satellite cells (MuSCs). • H19 partially colocalizes with MyoD transcripts. • H19 significantly stabilizes MyoD mRNA. • MyoD activates H19 by binding on its promoter and exons. [ABSTRACT FROM AUTHOR]

MicroRNAs are a class of small, non-coding RNAs that participate in the regulation of diverse biological processes including skeletal muscle development. However, the underlying molecular mechanisms are not fully understood, particularly in goat. Here, we identified goat miR-101a as a novel myogenic microRNA mediating myogenic differentiation. The expression of miR-101a was enriched in goat skeletal muscles and up-regulated during satellite cell differentiation. After transfection with a miR-101a mimic and culturing in differentiation medium, satellite cell differentiation was promoted, accompanied by a significant increase in mRNA expression of the myogenic marker, MyoG , and decreased expression of MyoD . In contrast, blocking the function of miR-101a with a 2′-O-methylated antisense oligonucleotide inhibitor repressed satellite cell differentiation. However, both gain- and loss-of-function studies demonstrated that miR-101a had no significant influence on satellite cell proliferation. Therefore, our results provide a new insight on miR-101a in the regulation of goat skeletal muscle satellite cell proliferation and differentiation. [ABSTRACT FROM AUTHOR]