Table 2_The role of goat FTO/IGF2BP1-mediated BCL11A m6A modification in intramuscular adipocyte differentiation.xls

Studies have shown that N6-methyladenosine (m6A) modification of mRNA exerts a key influence on adipocyte differentiation and lipid metabolism. However, whether m6A−modified mRNA regulates the differentiation of intramuscular adipocytes in goats remains unclear.</p>Methods<p>This study constructed the m6A methylation landscape during the differentiation of goat intramuscular adipocytes using MeRIP-seq and RNA-seq, and identified BCL11A as a key regulator exhibiting synchronized changes in both m6A modification and expression.</p>Results<p>Functional assays demonstrated that BCL11A promotes lipid accumulation and upregulates adipogenic markers (C/EBPα, PPARγ, SREBP1, FASN).

Mechanistically, the demethylase FTO directly targets the m6A site on BCL11A, while the reader protein IGF2BP1 recognizes this modification and reduces BCL11A mRNA stability. FTO promotes adipogenesis, whereas knockdown of IGF2BP1 shortens the half-life of BCL11A and inhibits differentiation.</p>Conclusion<p>These findings reveal that FTO and IGF2BP1 co-regulate the differentiation of intramuscular adipocytes through post-transcriptional modification of BCL11A, providing novel insights into m6A-mediated lipid deposition in goat muscle.</p>