ArticleThe Journal of cell biology2021
Glypican 4 mediates Wnt transport between germ layers via signaling filopodia.
Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Interactions between the bone morphogenetic protein and the planar cell polarity pathways lead to distinctive ethanol-induced facial defects.Alcohol, clinical & experimental research · 2025Article
- Synthetically programming natural cell-cell communication pathways for tissue engineering.Current opinion in biomedical engineering · 2024Article
- Gα13 controls pharyngeal endoderm convergence by regulating E-cadherin expression and RhoA activation.Development (Cambridge, England) · 2024Article
- Dichotomous Effects of Glypican-4 on Cancer Progression and Its Crosstalk with Oncogenes.International journal of molecular sciences · 2024Article
- Review
- Article
- Article
- Genome-wide identification of potential odontogenic genes involved in the dental epithelium-mesenchymal interaction during early odontogenesis.BMC genomics · 2023Article
- Review
- Coreceptor functions of cell surface heparan sulfate proteoglycans.American journal of physiology. Cell physiology · 2022Review
- Regulatory mechanisms of cytoneme-based morphogen transport.Cellular and molecular life sciences : CMLS · 2022Review
- Regulation of Wnt distribution and function by Drosophila glypicans.Journal of cell science · 2022Review
- Glypican 4 regulates planar cell polarity of endoderm cells by controlling the localization of Cadherin 2.Development (Cambridge, England) · 2021Article
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9 authors at 1 institution in 1 country.
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Abstract
Glypicans influence signaling pathways by regulating morphogen trafficking and reception. However, the underlying mechanisms in vertebrates are poorly understood. In zebrafish, Glypican 4 (Gpc4) is required for convergence and extension (C&E) of both the mesoderm and endoderm. Here, we show that transgenic expression of GFP-Gpc4 in the endoderm of gpc4 mutants rescued C&E defects in all germ layers. The rescue of mesoderm was likely mediated by Wnt5b and Wnt11f2 and depended on signaling filopodia rather than on cleavage of the Gpc4 GPI anchor. Gpc4 bound both Wnt5b and Wnt11f2 and regulated formation of the filopodia that transport Wnt5b and Wnt11f2 to neighboring cells. Moreover, this rescue was suppressed by blocking signaling filopodia that extend from endodermal cells. Thus, GFP-Gpc4-labeled protrusions that emanated from endodermal cells transported Wnt5b and Wnt11f2 to other germ layers, rescuing the C&E defects caused by a gpc4 deficiency. Our study reveals a new mechanism that could explain in vivo morphogen distribution involving Gpc4.
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