Skeletal muscle development relies on tightly coordinated transcriptional programs, yet the contribution of long non-coding RNAs (lncRNAs) to myogenesis remains largely unexplored. We previously demonstrated that the transcription factor TAp63γ is upregulated during myoblast differentiation and regulates the expression of genes involved in early stages of myogenic maturation. Here, combining transcriptome profiling with p63 ChIP-seq analysis in differentiating mouse myoblasts, we identify the lncRNA Airn as a direct transcriptional target of TAp63γ. Our findings position Airn as a previously unrecognized regulator of myogenic commitment that modulates both MyoD and MyoG expression at the mRNA and protein levels. Our work uncovers a novel TAp63γ–Airn axis essential for proper skeletal muscle differentiation and with potential relevance to muscle-wasting diseases.
Ciuffoli et al. (Thu,) studied this question.