ArticleDisease models & mechanisms2023
FZD2 regulates limb development by mediating β-catenin-dependent and -independent Wnt signaling pathways.
Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Diagnostic and mechanistic roles of miR-5584-5p in endometriosis via the FZD2-mediated Wnt/β-catenin EMT axis.Hereditas · 2026Article
- Clarifying Frizzled 2 function in development through genetically validated mouse models.Disease models & mechanisms · 2026Article
- Targeting frizzled receptors (FZDs) for anti-tumor therapy: From orthosteric to allosteric inhibition.Acta pharmaceutica Sinica. B · 2026Review
- Cis-regulatory evolution shapes facial diversity in birds and mammals.Science advances · 2026Article
- Targeting Wnt-driven metabolic adaptations in cancer: integrating glycolysis, glutaminolysis, IDO1-mediated immune evasion, and therapeutic delivery strategies.Frontiers in cell and developmental biology · 2025Review
- Preliminary exploration of potential biomarkers for heart failure and bipolar disorder: an exploratory study based on bioinformatics.Frontiers in psychiatry · 2025Article
- The role of the LncRNA XIST/miR-15a-5p/MN1 signaling axis in gender disparities in bladder cancer prognosis.Frontiers in immunology · 2025Article
- Craniofacial studies in chicken embryos confirm the pathogenicity of human FZD2 variants associated with Robinow syndrome.Disease models & mechanisms · 2024Article
- Successful therapeutic intervention in new mouse models of frizzled 2-associated congenital malformations.Development (Cambridge, England) · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Human Robinow syndrome (RS) and dominant omodysplasia type 2 (OMOD2), characterized by skeletal limb and craniofacial defects, are associated with heterozygous mutations in the Wnt receptor FZD2. However, as FZD2 can activate both canonical and non-canonical Wnt pathways, its precise functions and mechanisms of action in limb development are unclear. To address these questions, we generated mice harboring a single-nucleotide insertion in Fzd2 (Fzd2em1Smill), causing a frameshift mutation in the final Dishevelled-interacting domain. Fzd2em1Smill mutant mice had shortened limbs, resembling those of RS and OMOD2 patients, indicating that FZD2 mutations are causative. Fzd2em1Smill mutant embryos displayed decreased canonical Wnt signaling in developing limb mesenchyme and disruption of digit chondrocyte elongation and orientation, which is controlled by the β-catenin-independent WNT5A/planar cell polarity (PCP) pathway. In line with these observations, we found that disruption of FZD function in limb mesenchyme caused formation of shortened bone elements and defects in Wnt/β-catenin and WNT5A/PCP signaling. These findings indicate that FZD2 controls limb development by mediating both canonical and non-canonical Wnt pathways and reveal causality of pathogenic FZD2 mutations in RS and OMOD2 patients.
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