GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE330nnn/GSE330837/primary200OKTranscriptomicsMus musculus Genome binding/occupancy profiling by high throughput sequencingExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE330837GEOGSEfalseActive repression of muscle fate preserves neural lineage identity during cerebellum developmentCell fate commitment is commonly thought to entail progressive restriction of developmental potential, enforced by passive, heterochromatin-based silencing of alternative lineage programs. Here we show that maintenance of neural identity during cerebellum development instead requires active repression of a starkly divergent fate by the TEAD–INSM1 transcriptional complex. Loss of TEAD1/2 or INSM1 activates the myogenic master regulator Myod1, resulting in neural cells acquiring transcriptional, structural, and metabolic features of skeletal muscle cells. Deletion of Myod1 fully suppresses neural-to-muscle conversion while partially rescuing neural developmental defects. Our results uncover a latent alternative lineage during neurodevelopment and a surprising role for sequence-specific transcription factors in enforcing lineage boundaries, including those previously thought essentially unbreachable, with implications for understanding aberrant differentiation in disease contexts and cell-type evolution.2026/06/30GSE330837GSM9733392GSM9733391GSM9733394GSM9733393GSM9733390GSM9733399GSM9733396GSM9733395GSM9733398GSM9733397GSM9733408GSM9733407GSM9733409GSM9733404GSM9733403GSM9733406GSM9733405GSM9733400GSM9733402GSM9733401GSM9733372GSM9733419GSM9733418GSM9733415GSM9733414GSM9733417GSM9733416GSM9733378GSM9733411GSM9733410GSM9733377GSM9733413GSM9733379GSM9733412GSM9733374GSM9733373GSM9733376GSM9733375GSM9733381GSM9733380GSM9733383GSM9733382GSM9733422GSM9733389GSM9733421GSM9733388GSM9733424GSM9733423GSM9733385GSM9733384GSM9733387GSM9733420GSM973338634290330837Mus musculus[42182376]