ArticleHuman molecular genetics2017
Bimodal regulation of Dishevelled function by Vangl2 during morphogenesis.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Coupling mathematical modeling with a novel human intestinal stem cell system to understand feedback regulation during planar cell polarity.bioRxiv : the preprint server for biology · 2025Article
- Cell autonomous polarization by the planar cell polarity signaling pathway.Nature communications · 2025Article
- Cell autonomous polarization by the planar cell polarity signaling pathway.bioRxiv : the preprint server for biology · 2025Article
- Dact1 induces Dishevelled oligomerization to facilitate binding partner switch and signalosome formation during convergent extension.Nature communications · 2025Article
- Functional analysis of germline VANGL2 variants using rescue assays of vangl2 knockout zebrafish.Human molecular genetics · 2024Article
- An interaction between OTULIN and SCRIB uncovers roles for linear ubiquitination in planar cell polarity.Disease models & mechanisms · 2023Article
- A Van Gogh/Vangl tyrosine phosphorylation switch regulates its interaction with core Planar Cell Polarity factors Prickle and Dishevelled.PLoS genetics · 2023Article
- Wnt4 and ephrinB2 instruct apical constriction via Dishevelled and non-canonical signaling.Nature communications · 2023Article
- Article
- Cell non-autonomy amplifies disruption of neurulation by mosaic Vangl2 deletion in mice.Nature communications · 2021Article
- The Planar Polarity Component VANGL2 Is a Key Regulator of Mechanosignaling.Frontiers in cell and developmental biology · 2020Article
- Decoding Dishevelled-Mediated Wnt Signaling in Vertebrate Early Development.Frontiers in cell and developmental biology · 2020Review
- Vangl2-dependent regulation of membrane protrusions and directed migration requires a fibronectin extracellular matrix.Development (Cambridge, England) · 2018Article
- Cytoplasmic localization of GRHL3 upon epidermal differentiation triggers cell shape change for epithelial morphogenesis.Nature communications · 2018Article
- Planar Cell Polarity Signaling in Mammalian Cardiac Morphogenesis.Pediatric cardiology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Convergent extension (CE) is a fundamental morphogenetic mechanism that underlies numerous processes in vertebrate development, and its disruption can lead to human congenital disorders such as neural tube closure defects. The dynamic, oriented cell intercalation during CE is regulated by a group of core proteins identified originally in flies to coordinate epithelial planar cell polarity (PCP). The existing model explains how core PCP proteins, including Van Gogh (Vang) and Dishevelled (Dvl), segregate into distinct complexes on opposing cell cortex to coordinate polarity among static epithelial cells. The action of core PCP proteins in the dynamic process of CE, however, remains an enigma. In this report, we show that Vangl2 (Vang-like 2) exerts dual positive and negative regulation on Dvl during CE in both the mouse and Xenopus. We find that Vangl2 binds to Dvl to cell-autonomously promote efficient Dvl plasma membrane recruitment, a pre-requisite for PCP activation. At the same time, Vangl2 inhibits Dvl from interacting with its downstream effector Daam1 (Dishevelled associated activator of morphogenesis 1), and functionally suppresses Dvl → Daam1 cascade during CE. Our finding uncovers Vangl2-Dvl interaction as a key bi-functional switch that underlies the central logic of PCP signaling during morphogenesis, and provides new insight into PCP-related disorders in humans.
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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.