{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE309nnn/GSE309306/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE309306"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Substantial Adaptability of Mononuclear Polyploid Cardiomyocytes Revealed by Perinatal Loss of Chaf1a","description":"Here, we show that chromatin assembly factor 1 subunit A (Chaf1a), a key regulator of nucleosome deposition during DNA replication, is essential for postnatal cardiomyocyte proliferation and binucleation. Using cardiomyocyte-specific Chaf1a knockout mice (Myh6-Cre; Chaf1af/f), we demonstrate that Chaf1a deficiency disrupts karyokinesis, leading to a marked increase in the proportion of mononuclear polyploid cardiomyocytes and a reduction in binucleated cells. This results in nearly 50% fewer cardiomyocytes, yet strikingly, the hearts preserve baseline function through substantial compensatory hypertrophy without significant fibrosis. Notably, following cardiac apex resection, neonatal Myh6-Cre; Chaf1af/f mice fail to regenerate myocardium, highlighting the essential role of Chaf1a in cardiac regeneration.","dates":{"publication":"2026/07/17"},"accession":"GSE309306","cross_references":{"GSM":["GSM9484096","GSM9484095","GSM9264589","GSM9484098","GSM9264588","GSM9484097","GSM9264587","GSM9264586","GSM9264591","GSM9264590","GSM9484100","GSM9484099"],"GPL":["24247"],"GSE":["309306"],"taxon":["Mus musculus"]}}