{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Le Pabic P"],"funding":["NIDCR NIH HHS"],"pagination":["e1004726"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4207671"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(10)"],"pubmed_abstract":["Organogenesis requires coordinated regulation of cellular differentiation and morphogenesis. Cartilage cells in the vertebrate skeleton form polarized stacks, which drive the elongation and shaping of skeletal primordia. Here we show that an atypical cadherin, Fat3, and its partner Dachsous-2 (Dchs2), control polarized cell-cell intercalation of cartilage precursors during craniofacial development. In zebrafish embryos deficient in Fat3 or Dchs2, chondrocytes fail to stack and misregulate expression of sox9a. Similar morphogenetic defects occur in rerea/atr2a-/- mutants, and Fat3 binds REREa, consistent with a model in which Fat3, Dchs2 and REREa interact to control polarized cell-cell intercalation and simultaneously control differentiation through Sox9. Chimaeric analyses support such a "],"journal":["PLoS genetics"],"pubmed_title":["Fat-Dachsous signaling coordinates cartilage differentiation and polarity during craniofacial development."],"pmcid":["PMC4207671"],"funding_grant_id":["F32DE21308","R01 DE013828","R01DE13828","F32 DE021308"],"pubmed_authors":["Le Pabic P","Ng C","Schilling TF"],"additional_accession":[]},"is_claimable":false,"name":"Fat-Dachsous signaling coordinates cartilage differentiation and polarity during craniofacial development.","description":"Organogenesis requires coordinated regulation of cellular differentiation and morphogenesis. Cartilage cells in the vertebrate skeleton form polarized stacks, which drive the elongation and shaping of skeletal primordia. Here we show that an atypical cadherin, Fat3, and its partner Dachsous-2 (Dchs2), control polarized cell-cell intercalation of cartilage precursors during craniofacial development. In zebrafish embryos deficient in Fat3 or Dchs2, chondrocytes fail to stack and misregulate expression of sox9a. Similar morphogenetic defects occur in rerea/atr2a-/- mutants, and Fat3 binds REREa, consistent with a model in which Fat3, Dchs2 and REREa interact to control polarized cell-cell intercalation and simultaneously control differentiation through Sox9. Chimaeric analyses support such a ","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Oct","modification":"2025-04-18T16:19:14.074Z","creation":"2019-03-27T01:38:16Z"},"accession":"S-EPMC4207671","cross_references":{"pubmed":["25340762"],"doi":["10.1371/journal.pgen.1004726"]}}