GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE327nnn/GSE327304/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327304GEOGSEfalseTranscriptomic characterization of Wild type mouse Embryonic Stem Cells (mESCs), β-actin Knock out mESC and upon rescue with a nuclear localization signal β-actinPluripotency and lineage commitment in embryonic stem cells depend on coordinated regulation of chromatin architecture and extracellular matrix (ECM) signaling. Here, we identify nuclear β-actin as a key regulator linking these processes in mouse embryonic stem cells. Loss of β-actin disrupts core pluripotency factors, including Oct4 and Sox2, and causes broad transcriptional changes, while nuclear re-expression rescues these defects. Chromatin accessibility analysis revealed reduced accessibility at regulatory regions of pluripotency genes, consistent with impaired chromatin remodeling. β-actin depletion also altered ECM-related gene expression, matrix properties, and cellular biomechanics, leading to impaired self-renewal, skewed lineage specification, and defective differentiation, particularly reduced neuronal potential and increased mesodermal-like fate bias. In vivo, β-actin loss restricted teratoma growth and compromised tri-lineage differentiation. Together, these results define nuclear β-actin as an important regulator of chromatin accessibility, ECM-dependent signaling, and stem cell fate.2026/04/13GSE327304GSM9653176GSM9653154GSM9653177GSM9653155GSM9653156GSM9653178GSM9653179GSM9653157GSM9653172GSM9653173GSM9653174GSM9653152GSM9653153GSM9653175GSM9653158GSM9653159GSM9653170GSM9653171GSM9653165GSM9653166GSM9653167GSM9653168GSM9653183GSM9653161GSM9653162GSM9653184GSM9653163GSM9653164GSM9653169GSM9653180GSM9653181GSM9653182GSM965316024247327304Mus musculus