{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE308nnn/GSE308927/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Ovis aries"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE308927"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell transcriptomic profiling of Hulunbuir short-tailed sheep and Hu sheep embryos at E16 and E19 reveals T gene mutation-mediated regulatory mechanisms underlying tail length phenotype","description":"This study presents a comprehensive single-cell RNA sequencing (scRNA-seq) atlas of embryonic development in two distinct Chinese sheep breeds: the cold-adapted Hulunbuir short-tailed sheep (HSTS) and the heat-tolerant Hu sheep (HS). We profiled embryos at two critical developmental timepoints—16 and 19 days post-insemination—to investigate the cellular heterogeneity and molecular mechanisms underlying tail length dimorphism. Our analysis identified 12–15 distinct cell types across samples and revealed MDK_ITGA6+ITGB1 as a central ligand-receptor pair in intercellular communication. We observed that HSTS embryos exhibit premature degeneration of the apical ectodermal ridge (AER), driven by a loss-of-function mutation in the T gene (c.G334T), which dysregulates BMP and FGF signaling pathways. Functional validation in a T mutant mouse model confirmed the role of this mutation in tail shortening. These findings provide insight into the genetic and cellular basis of adaptive tail morphology and offer potential targets for livestock breeding.","dates":{"publication":"2026/06/18"},"accession":"GSE308927","cross_references":{"GSM":["GSM9256371","GSM9256370","GSM9256369"],"GPL":["27721"],"GSE":["308927"],"taxon":["Ovis aries"],"PMID":["[42278180]"]}}