Molecular Characterizations of FAM13A and Its Functional Role in Inhibiting the Differentiation of Goat Intramuscular Adipocytes through RIG-I Receptor Signaling Pathway

The aim of this study was to elucidate the effect of <i>FAM13A</i> on the differentiation of goat intramuscular precursor adipocytes and its mechanism of action. Here, we cloned the CDS region 2094 bp of the goat <i>FAM13A</i> gene, encoding a total of 697 amino acid residues. Functionally, overexpression of <i>FAM13A</i> inhibited the differentiation of goat intramuscular adipocytes with a concomitant reduction in lipid droplets, whereas interference with <i>FAM13A</i> expression promoted the differentiation of goat intramuscular adipocytes. To further investigate the mechanism of <i>FAM13A</i> inhibiting adipocyte differentiation, 104 differentially expressed genes were screened by RNA-seq, including 95 up-regulated genes and 9 down-regulated genes. KEGG analysis found that the RIG-I receptor signaling pathway, NOD receptor signaling pathway and toll-like receptor signaling pathway may affect adipogenesis. We selected the RIG-I receptor signaling pathway enriched with more differential genes as a potential adipocyte differentiation signaling pathway for verification. Convincingly, the RIG-I like receptor signaling pathway inhibitor (HY-P1934A) blocked this pathway to save the phenotype observed in intramuscular adipocyte with <i>FAM13A</i> overexpression. Finally, the upstream miRNA of <i>FAM13A</i> was predicted, and the targeted inhibition of miR-21-5p on the expression of <i>FAM13A</i> gene was confirmed. In this study, it was found that FAM13A inhibited the differentiation of goat intramuscular adipocytes through the RIG-I receptor signaling pathway, and the upstream miRNA of <i>FAM13A</i> (miR-21-5p) promoted the differentiation of goat intramuscular adipocytes. This work extends the genetic regulatory network of IMF deposits and provides theoretical support for improving human health and meat quality from the perspective of IMF deposits.