ArticleDisease models & mechanisms2022
Vangl2-environment interaction causes severe neural tube defects, without abnormal neuroepithelial convergent extension.
Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 18 citations in OpenAlex.
- Germline and Embryonic Mechanisms in the Epigenetic Inheritance of Neurodevelopmental and Cognitive Traits in Mammals.Biomolecules · 2026Review
- The role of chrysanthemum phytochemicals in neural tube development: a narrative review of underlying mechanisms.Frontiers in cell and developmental biology · 2026Review
- Fold-and-fuse neurulation in zebrafish requires vangl2.Developmental biology · 2025Article
- Integrative Analysis of Key Signalling Pathways in Neural Tube Defects: From Molecular Mechanisms to Therapeutic Strategies.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2025Review
- Monitoring the Mechanical Evolution of Tissue During Neural Tube Closure of Chick Embryo.Journal of visualized experiments : JoVE · 2023Article
- Morphological phenotyping after mouse whole embryo culture.Frontiers in cell and developmental biology · 2023Review
- Progress in Modeling Neural Tube Development and Defects by Organoid Reconstruction.Neuroscience bulletin · 2022Review
- Somitic mesoderm morphogenesis is necessary for neural tube closure during Xenopus development.Frontiers in cell and developmental biology · 2022Article
- The bidirectional relationship between cilia and PCP signaling pathway core protein Vangl2.Science progressReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Planar cell polarity (PCP) signalling is vital for initiation of mouse neurulation, with diminished convergent extension (CE) cell movements leading to craniorachischisis, a severe neural tube defect (NTD). Some humans with NTDs also have PCP gene mutations but these are heterozygous, not homozygous as in mice. Other genetic or environmental factors may interact with partial loss of PCP function in human NTDs. We found that reduced sulfation of glycosaminoglycans interacts with heterozygosity for the Lp allele of Vangl2 (a core PCP gene), to cause craniorachischisis in cultured mouse embryos, with rescue by exogenous sulphate. We hypothesized that this glycosaminoglycan-PCP interaction may regulate CE, but, surprisingly, DiO labelling of the embryonic node demonstrates no abnormality of midline axial extension in sulfation-depleted Lp/+ embryos. Positive-control Lp/Lp embryos show severe CE defects. Abnormalities were detected in the size and shape of somites that flank the closing neural tube in sulfation-depleted Lp/+ embryos. We conclude that failure of closure initiation can arise by a mechanism other than faulty neuroepithelial CE, with possible involvement of matrix-mediated somite expansion, adjacent to the closing neural tube.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.