{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shull LC"],"funding":["National Institute of Neurological Disorders and Stroke","NIDCR NIH HHS","National Institute of Dental and Craniofacial Research","NINDS NIH HHS","NCI NIH HHS"],"pagination":["dev200082"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8918787"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["149(4)"],"pubmed_abstract":["Cranial neural crest cell (NCC)-derived chondrocyte precursors undergo a dynamic differentiation and maturation process to establish a scaffold for subsequent bone formation, alterations in which contribute to congenital birth defects. Here, we demonstrate that transcription factor and histone methyltransferase proteins Prdm3 and Prdm16 control the differentiation switch of cranial NCCs to craniofacial cartilage. Loss of either paralog results in hypoplastic and disorganized chondrocytes due to impaired cellular orientation and polarity. We show that these proteins regulate cartilage differentiation by controlling the timing of Wnt/β-catenin activity in strikingly different ways: Prdm3 represses whereas Prdm16 activates global gene expression, although both act by regulating Wnt enhanceoso"],"journal":["Development (Cambridge, England)"],"pubmed_title":["PRDM paralogs antagonistically balance Wnt/β-catenin activity during craniofacial chondrocyte differentiation."],"pmcid":["PMC8918787"],"funding_grant_id":["P30 CA046934","P30 NS048154","R01 DE030377","R01 DE024034","F32 DE029099"],"pubmed_authors":["Shull LC","Kim HM","Jones K","Lencer ES","Goyama S","Costello JC","Artinger KB","Kurokawa M"],"additional_accession":[]},"is_claimable":false,"name":"PRDM paralogs antagonistically balance Wnt/β-catenin activity during craniofacial chondrocyte differentiation.","description":"Cranial neural crest cell (NCC)-derived chondrocyte precursors undergo a dynamic differentiation and maturation process to establish a scaffold for subsequent bone formation, alterations in which contribute to congenital birth defects. Here, we demonstrate that transcription factor and histone methyltransferase proteins Prdm3 and Prdm16 control the differentiation switch of cranial NCCs to craniofacial cartilage. Loss of either paralog results in hypoplastic and disorganized chondrocytes due to impaired cellular orientation and polarity. We show that these proteins regulate cartilage differentiation by controlling the timing of Wnt/β-catenin activity in strikingly different ways: Prdm3 represses whereas Prdm16 activates global gene expression, although both act by regulating Wnt enhanceoso","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2026-05-29T10:37:35.801Z","creation":"2025-02-19T02:23:51.451Z"},"accession":"S-EPMC8918787","cross_references":{"pubmed":["35132438"],"doi":["10.1242/dev.200082"]}}