ArticleNature communications2014
ptk7 mutant zebrafish models of congenital and idiopathic scoliosis implicate dysregulated Wnt signalling in disease.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 169 citations in OpenAlex.
- Massively parallel characterization of adolescent idiopathic scoliosis risk variants.Genome research · 2026Article
- Serotonergic Control of Spine Morphology During Growth in Zebrafish.bioRxiv : the preprint server for biology · 2026Article
- Development of the zebrafish foveal analogue: a quantitative atlas of high-acuity zone growth and retinal regionalisation.Biology open · 2026Article
- Distinct regulation of Wnt signaling and EPZ5676 governs human UiPSM reprogramming via the CDX2/T/TBX6 core axis.Cell regeneration (London, England) · 2026Article
- The role of genetics and molecular mechanisms in early onset scoliosis.Journal of clinical orthopaedics and trauma · 2026Review
- Impact of maternal compensation on developmental phenotypes in a zebrafish model of severe congenital muscular dystrophy.PLoS genetics · 2026Article
- Early pharmacological blockade of the CXCL12-CXCR4 axis attenuates vertebral hypercalcification in a zebrafish model of pseudoxanthoma elasticum.Biochemistry and biophysics reports · 2025Article
- The importance of imperfect pre-clinical models in adolescent idiopathic scoliosis.Disease models & mechanisms · 2025Review
- C-mannosyltransferase DPY19L1L-mediated Reissner Fiber formation is critical for zebrafish (Science advances · 2025Article
- Difference in clinical presentation and surgical outcomes in pediatric and adult patients with Chiari malformation type 1: a single center retrospective study.Acta neurochirurgica · 2025Article
- Air-liquid interface culture for live analysis of zebrafish vertebral growth.microPublication biology · 2025Article
- Spinal scoliosis: insights into developmental mechanisms and animal models.Spine deformity · 2025Review
- Scoliosis as a Paradigm of Pathological Spinal Curvature: Molecular Mechanisms and Imaging Innovations : Molecular and Imaging Insights in Scoliosis.Galen medical journal · 2025Review
- Planar cell polarity zebrafish models of congenital scoliosis reveal underlying defects in notochord morphogenesis.Development (Cambridge, England) · 2024Article
- Article
- Nkd1 functions downstream of Axin2 to attenuate Wnt signaling.Molecular biology of the cell · 2024Article
- Article
- Recent insights into the therapeutic strategies targeting the pseudokinase PTK7 in cancer.Oncogene · 2024Review
- Molecular landscape of congenital vertebral malformations: recent discoveries and future directions.Orphanet journal of rare diseases · 2024Review
- Association of genetic variation ineLife · 2024Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Scoliosis is a complex genetic disorder of the musculoskeletal system, characterized by three-dimensional rotation of the spine. Curvatures caused by malformed vertebrae (congenital scoliosis (CS)) are apparent at birth. Spinal curvatures with no underlying vertebral abnormality (idiopathic scoliosis (IS)) most commonly manifest during adolescence. The genetic and biological mechanisms responsible for IS remain poorly understood due largely to limited experimental models. Here we describe zygotic ptk7 (Zptk7) mutant zebrafish, deficient in a critical regulator of Wnt signalling, as the first genetically defined developmental model of IS. We identify a novel sequence variant within a single IS patient that disrupts PTK7 function, consistent with a role for dysregulated Wnt activity in disease pathogenesis. Furthermore, we demonstrate that embryonic loss-of-gene function in maternal-zygotic ptk7 mutants (MZptk7) leads to vertebral anomalies associated with CS. Our data suggest novel molecular origins of, and genetic links between, congenital and idiopathic forms of disease.
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