{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Farmer DT"],"funding":["NIDCR NIH HHS","Howard Hughes Medical Institute","Burroughs Wellcome Fund","U.S. Department of Health & Human Services | National Institutes of Health (NIH)","U.S. Department of Health & Human Services | National Institutes of Health"],"pagination":["6948"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11322166"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Cranial sutures separate neighboring skull bones and are sites of bone growth. A key question is how osteogenic activity is controlled to promote bone growth while preventing aberrant bone fusions during skull expansion. Using single-cell transcriptomics, lineage tracing, and mutant analysis in zebrafish, we uncover key developmental transitions regulating bone formation at sutures during skull expansion. In particular, we identify a subpopulation of mesenchyme cells in the mid-suture region that upregulate a suite of genes including BMP antagonists (e.g. grem1a) and pro-angiogenic factors. Lineage tracing with grem1a:nlsEOS reveals that this mid-suture subpopulation is largely non-osteogenic. Moreover, combinatorial mutation of BMP antagonists enriched in this mid-suture subpopulation results in increased BMP signaling in the suture, misregulated bone formation, and abnormal suture morphology. These data reveal establishment of a non-osteogenic mesenchyme population in the mid-suture region that restricts bone formation through local BMP antagonism, thus ensuring proper suture morphology."],"journal":["Nature communications"],"pubmed_title":["Cellular transitions during cranial suture establishment in zebrafish."],"pmcid":["PMC11322166"],"funding_grant_id":["5R01DE026339","R01 DE026339"],"pubmed_authors":["Xu P","Teng CS","Hernandez-Trejo J","Arata C","Maxson RE","Dukov JE","Crump JG","Farmer DT","Chen HJ"],"additional_accession":[]},"is_claimable":false,"name":"Cellular transitions during cranial suture establishment in zebrafish.","description":"Cranial sutures separate neighboring skull bones and are sites of bone growth. A key question is how osteogenic activity is controlled to promote bone growth while preventing aberrant bone fusions during skull expansion. Using single-cell transcriptomics, lineage tracing, and mutant analysis in zebrafish, we uncover key developmental transitions regulating bone formation at sutures during skull expansion. In particular, we identify a subpopulation of mesenchyme cells in the mid-suture region that upregulate a suite of genes including BMP antagonists (e.g. grem1a) and pro-angiogenic factors. Lineage tracing with grem1a:nlsEOS reveals that this mid-suture subpopulation is largely non-osteogenic. Moreover, combinatorial mutation of BMP antagonists enriched in this mid-suture subpopulation results in increased BMP signaling in the suture, misregulated bone formation, and abnormal suture morphology. These data reveal establishment of a non-osteogenic mesenchyme population in the mid-suture region that restricts bone formation through local BMP antagonism, thus ensuring proper suture morphology.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2025-04-19T20:38:38.303Z","creation":"2025-04-19T20:38:38.303Z"},"accession":"S-EPMC11322166","cross_references":{"pubmed":["39138165"],"doi":["10.1038/s41467-024-50780-5"]}}