ArticleDevelopment (Cambridge, England)2023
The non-canonical Wnt receptor Ror2 is required for cartilage cell polarity and morphogenesis of the craniofacial skeleton in zebrafish.
Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
7 citing papers in PubMed, 13 citations in OpenAlex.
- Optimised genome editing for precise DNA insertion and substitution using prime editors in zebrafish.eLife · 2026Article
- Analysis of cranial tenocyte heterogeneity reveals a role for Wnt signaling in tendon attachments.Development (Cambridge, England) · 2026Article
- Loss of Stat3 in Prx1Advanced biology · 2025Article
- Non-canonical Wnt signaling triggered by WNT2B drives adrenal aldosterone production.bioRxiv : the preprint server for biology · 2024Article
- Role of the Ror family receptors in Wnt5a signaling.In vitro cellular & developmental biology. Animal · 2024Review
- Transforming growth factor beta signaling and craniofacial development: modeling human diseases in zebrafish.Frontiers in cell and developmental biology · 2024Review
- Loss ofBiomolecules · 2023Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Non-canonical/β-catenin-independent Wnt signaling plays crucial roles in tissue/cell polarity in epithelia, but its functions have been less well studied in mesenchymal tissues, such as the skeleton. Mutations in non-canonical Wnt signaling pathway genes cause human skeletal diseases such as Robinow syndrome and Brachydactyly Type B1, which disrupt bone growth throughout the endochondral skeleton. Ror2 is one of several non-canonical Wnt receptor/co-receptors. Here, we show that ror2-/- mutant zebrafish have craniofacial skeletal defects, including disruptions of chondrocyte polarity. ror1-/- mutants appear to be phenotypically wild type, but loss of both ror1 and ror2 leads to more severe cartilage defects, indicating partial redundancy. Skeletal defects in ror1/2 double mutants resemble those of wnt5b-/- mutants, suggesting that Wnt5b is the primary Ror ligand in zebrafish. Surprisingly, the proline-rich domain of Ror2, but not its kinase domain, is required to rescue its function in mosaic transgenic experiments in ror2-/- mutants. These results suggest that endochondral bone defects in ROR-related human syndromes reflect defects in cartilage polarity and morphogenesis.
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Registered trials
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