{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nestor-Bergmann A"],"funding":["CNRS","University of Cambridge Herchel Smith Fund","University of Sheffield","Rhône-Alpes region","Labex","Wellcome Trust","Biotechnology and Biological Sciences Research Council"],"pagination":["e1009812"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8887740"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(1)"],"pubmed_abstract":["Cell intercalation is a key cell behaviour of morphogenesis and wound healing, where local cell neighbour exchanges can cause dramatic tissue deformations such as body axis extension. Substantial experimental work has identified the key molecular players facilitating intercalation, but there remains a lack of consensus and understanding of their physical roles. Existing biophysical models that represent cell-cell contacts with single edges cannot study cell neighbour exchange as a continuous process, where neighbouring cell cortices must uncouple. Here, we develop an Apposed-Cortex Adhesion Model (ACAM) to understand active cell intercalation behaviours in the context of a 2D epithelial tissue. The junctional actomyosin cortex of every cell is modelled as a continuous viscoelastic rope-loo"],"journal":["PLoS computational biology"],"pubmed_title":["Adhesion-regulated junction slippage controls cell intercalation dynamics in an Apposed-Cortex Adhesion Model."],"pmcid":["PMC8887740"],"funding_grant_id":["ANR-11-LABX-0030","Grant CPER07\\_13 CIRA","207553Z17Z","BB/R016925/1","099234Z12Z","Vice-Chancellor’s Fellowship","BB/R000395/1","PICS CNRS travel grant"],"pubmed_authors":["Nestor-Bergmann A","Hervieux N","Etienne J","Blanchard GB","Fletcher AG","Sanson B"],"additional_accession":[]},"is_claimable":false,"name":"Adhesion-regulated junction slippage controls cell intercalation dynamics in an Apposed-Cortex Adhesion Model.","description":"Cell intercalation is a key cell behaviour of morphogenesis and wound healing, where local cell neighbour exchanges can cause dramatic tissue deformations such as body axis extension. Substantial experimental work has identified the key molecular players facilitating intercalation, but there remains a lack of consensus and understanding of their physical roles. Existing biophysical models that represent cell-cell contacts with single edges cannot study cell neighbour exchange as a continuous process, where neighbouring cell cortices must uncouple. Here, we develop an Apposed-Cortex Adhesion Model (ACAM) to understand active cell intercalation behaviours in the context of a 2D epithelial tissue. The junctional actomyosin cortex of every cell is modelled as a continuous viscoelastic rope-loo","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2025-04-04T08:41:15.24Z","creation":"2025-04-04T08:41:15.24Z"},"accession":"S-EPMC8887740","cross_references":{"pubmed":["35089922"],"doi":["10.1371/journal.pcbi.1009812"]}}