ArticleThe Journal of cell biology2026
Actomyosin contractility and a threshold of cadherin cell adhesion are required during tissue fusion.
Article in The Journal of cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis.Development (Cambridge, England) · 2026Article
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Authors and funding
5 authors.
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Abstract
Tissue fusion is integral to mammalian morphogenesis, and its failure is a significant cause of structural anomalies, yet the underlying cellular mechanisms are incompletely understood. We examine cellular drivers of upper lip fusion in the mammalian embryo by establishing a live-imaging modality, revealing specific enrichment of F-actin that propagates in multicellular cables anchored at the fusion site. Actomyosin contractility drives lip fusion, and its pharmacological or genetic attenuation results in failed fusion and cleft lip. Generating a series of mice deficient in specific p120-catenin molecular functions, we reveal that p120-catenin binding to RhoA and Kaiso is dispensable during mammalian development, while stabilization of cadherins is crucial. Through generating an allelic series of new compound P-cadherin/E-cadherin mouse mutations disrupting combined cadherin levels, we unveil an elevated cadherin cell adhesion threshold requirement specific to upper lip fusion. Finally, we identify CDH3 variants in individuals with cleft lip, supporting the relevance of this mechanism in human tissue fusion.
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