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Related Concept Videos

Canonical Wnt Signaling Pathway02:54

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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Related Experiment Video

Updated: Oct 9, 2025

Studying Wnt Signaling During Patterning of Conducting Airways
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Epithelial Wntless regulates postnatal alveologenesis.

Yinshan Fang1, Hongxia Shao1,2, Qi Wu2

  • 1Division of Digestive and Liver Diseases, Department of Medicine, Columbia Center for Human Development, Columbia University Medical Center, New York, NY 10032, USA.

Development (Cambridge, England)
|December 21, 2021
PubMed
Summary

Epithelial Wnt signaling is vital for lung development. Disrupting Wntless (Wls) impairs alveolar formation and promotes fibrosis by affecting mesenchymal cell differentiation and endothelial-to-mesenchymal transition (EndMT).

Keywords:
AlveologenesisBronchopulmonary dysplasiaEndotheliumLungWntWntless

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Area of Science:

  • Pulmonary biology
  • Developmental biology
  • Cell signaling

Background:

  • Alveologenesis, the formation of lung alveoli, requires intricate epithelial-mesenchymal interactions.
  • The precise molecular regulators of these interactions during lung development remain incompletely understood.

Purpose of the Study:

  • To investigate the role of epithelial-derived Wnt signaling in neonatal lung alveolar development.
  • To elucidate the molecular mechanisms linking epithelial Wnt production to mesenchymal cell differentiation and alveolar structure.

Main Methods:

  • Utilized conditional knockout mouse models (Sftpc-Cre/Nkx2.1-Cre; Wlsloxp/loxp and Ager-CreER; Wlsloxp/loxp) to delete Wntless (Wls) in specific cell populations.
  • Analyzed lung histology, cell populations (α-SMA+ cells), collagen deposition, and fibrotic responses following bleomycin challenge.

Main Results:

  • Epithelial Wntless (Wls) deletion disrupted alveolar saccule formation, leading to enlarged airspaces.
  • Persistent α-SMA+ mesenchymal cells and increased collagen deposition were observed in mutants.
  • Endothelial-to-mesenchymal transition (EndMT) was identified in α-SMA+ cells within the affected alveoli.
  • Mutants showed exacerbated lung fibrosis after bleomycin injury.

Conclusions:

  • Epithelial-derived Wnts are essential for proper mesenchymal cell differentiation during neonatal alveologenesis.
  • Disruption of Wnt signaling contributes to persistent mesenchymal phenotypes and impaired lung development.
  • These findings highlight a critical role for Wnt signaling in regulating the epithelial-mesenchymal crosstalk necessary for lung maturation and fibrosis susceptibility.