GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE286nnn/GSE286164/primaryOK200Methylation profilingHomo sapiensMethylation profiling by arrayhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE286164GEOGSEfalseEpigenomic-transcriptional network during neural crest cell differentiation [DNA methylation]Neural crest cells (NCCs) originate from the neural tube during early embryogenesis, and they are a pivotal cell population involved in vertebrate development. NCCs are mainly divided into cranial NCCs (cNCCs) and trunk NCCs (tNCCs), which subsequently differentiate into diverse tissues and organs. Proper differentiation and fate determination into NCCs are essential for normal development and survival of individuals, and abnormal differentiation of NCCs can lead to various diseases such as cardiac disorders and tumors. Epigenetic mechanisms, including histone modification and DNA methylation, are crucial for regulating NCC differentiation. However, the specific mechanisms of DNA methylation underlying the differentiation of cNCCs and tNCCs remain poorly understood. This study aimed to address this knowledge gap by comparing the differentiation mechanisms of cranial and trunk NCCs derived from human induced pluripotent stem cells. Through integrated analysis of the transcriptome and DNA methylome data, we found that along with differentiation, DNA demethylation upstream of the transcription start sites of myocyte enhancer factor 2C (MEF2C) in cNCCs and thyroid hormone receptor alpha-2 (THRA2) in tNCCs led to increased expression of these genes. Furthermore, MEF2C and THRA2 were found to potentially regulate NCC markers. Our findings contribute to a detailed understanding of regulatory mechanisms of DNA methylation in normal NCC differentiation and may provide insights into the pathogenesis of NCC-related diseases such as neuroblastoma.2026/04/26GSE286164GSM8720036GSM8720035GSM8720034GSM8720033GSM8720032GSM8720031GSM8720030GSM8720029GSM872002821145286164Homo sapiens