{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315558/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Danio rerio"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315558"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Myocardial Hand2 regulates cardiac trabeculation","description":"During cardiac trabeculation, some compact layer cardiomyocytes delaminate to form complex multicellular ridges in the ventricular wall. However, much remains to be understood about the cellular and molecular mechanisms underlying this process. Here, we first show that the bHLH transcription factor gene hand2, which plays key roles in cardiac development, is expressed in both the myocardium and endocardium in zebrafish embryos. Since hand2-null zebrafish fail to form a heart tube, we generated a hand2 floxed allele to dissect its function in specific cell types. Deleting hand2 in cardiomyocytes (CMs) leads to specific defects in trabecular formation, specifically premature CM delamination and subsequently a failure to form clear multicellular ridges. Using genetic mosaics, we found that Hand2 regulates CM behavior cell-autonomously. Notably, we also observed increased CM proliferation upon deleting hand2 in the myocardium. Furthermore, we found that hand2-/- CMs, unlike their wild-type counterparts, do not require Erbb2 to delaminate. Altogether, these data provide additional insight into the multiple roles of Hand2 during cardiac development.","dates":{"publication":"2026/10/02"},"accession":"GSE315558","cross_references":{"GSM":["GSM9431098","GSM9431097","GSM9431094","GSM9431093","GSM9431096","GSM9431095"],"GPL":["30614"],"GSE":["315558"],"taxon":["Danio rerio"]}}