ArticleDevelopmental biology2015
Wt1 and β-catenin cooperatively regulate diaphragm development in the mouse.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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
30 citing papers in PubMed, 40 citations in OpenAlex.
- Modeling patient variants of Cnot1 and Cdc42bpb results in distinct forms of congenital diaphragmatic hernia in mice.Human molecular genetics · 2026Article
- A who's who of cell types in skeletal muscle.Communications biology · 2026Review
- Modeling patient variants ofbioRxiv : the preprint server for biology · 2026Article
- HALO: hierarchical causal modeling for single cell multi-omics data.Nature communications · 2025Article
- The etiology of congenital diaphragmatic hernia: the retinoid hypothesis 20 years later.Pediatric research · 2024Review
- Connecting clinical, environmental, and genetic factors point to an essential role for vitamin A signaling in the pathogenesis of congenital diaphragmatic hernia.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Crosstalk between β-catenin and WT1 signaling activity in acute myeloid leukemia.Haematologica · 2023Article
- The role of genes and environment in the etiology of congenital diaphragmatic hernias.Current topics in developmental biology · 2023Review
- Article
- Global gene expression profiling in congenital diaphragmatic hernia (CDH) patients.Functional & integrative genomics · 2022Article
- Cellular, molecular, and metabolic aspects of developing lungs in congenital diaphragmatic hernia.Frontiers in pediatrics · 2022Review
- Genetically Modified Mouse Models of Congenital Diaphragmatic Hernia: Opportunities and Limitations for Studying Altered Lung Development.Frontiers in pediatrics · 2022Review
- Defective mesothelium and limited physical space are drivers of dysregulated lung development in a genetic model of congenital diaphragmatic hernia.Development (Cambridge, England) · 2021Article
- Morphofunctional Characterization of Different Tissue Factors in Congenital Diaphragmatic Hernia Affected Tissue.Diagnostics (Basel, Switzerland) · 2021Article
- Resolving the heterogeneity of diaphragmatic mesenchyme: a novel mouse model of congenital diaphragmatic hernia.Disease models & mechanisms · 2021Article
- Cellular Origin(s) of Congenital Diaphragmatic Hernia.Frontiers in pediatrics · 2021Review
- Unraveling the Genetics of Congenital Diaphragmatic Hernia: An Ongoing Challenge.Frontiers in pediatrics · 2021Review
- β-catenin regulates muscle glucose transport via actin remodelling and M-cadherin binding.Molecular metabolism · 2020Article
- Congenital diaphragmatic hernia as a prominent feature of a SPECC1L-related syndrome.American journal of medical genetics. Part A · 2020Article
- Cell culture system to assay candidate genes and molecular pathways implicated in congenital diaphragmatic hernias.Developmental biology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The developing diaphragm consists of various differentiating cell types, many of which are not well characterized during organogenesis. One important but incompletely understood tissue, the diaphragmatic mesothelium, is distinctively present from early stages of development. Congenital Diaphragmatic Hernia (CDH) occurs in humans when diaphragm tissue is lost during development, resulting in high morbidity and mortality postnatally. We utilized a Wilms Tumor 1 (Wt1) mutant mouse model to investigate the involvement of the mesothelium in normal diaphragm signaling and development. Additionally, we developed and characterized a Wt1(CreERT2)-driven β-catenin loss-of-function model of CDH after finding that canonical Wnt signaling and β-catenin are reduced in Wt1 mutant mesothelium. Mice with β-catenin loss or constitutive activation induced in the Wt1 lineage are only affected when tamoxifen injection occurs between E10.5 and E11.5, revealing a critical time-frame for Wt1/ β-catenin activity. Conditional β-catenin loss phenocopies the Wt1 mutant diaphragm defect, while constitutive activation of β-catenin on the Wt1 mutant background is sufficient to close the diaphragm defect. Proliferation and apoptosis are affected, but primarily these genetic manipulations appear to lead to a change in normal diaphragm differentiation. Our data suggest a fundamental role for mesothelial signaling in proper formation of the diaphragm.
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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.