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Related Concept Videos

Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

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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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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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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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Notch Signaling Pathway03:14

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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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Pleiotropy is the phenomenon in which a single gene impacts multiple, seemingly unrelated phenotypic traits. For example, defects in the SOX10 gene cause Waardenburg Syndrome Type 4, or WS4, which can cause defects in pigmentation, hearing impairments, and an absence of intestinal contractions necessary for elimination. This diversity of phenotypes results from the expression pattern of SOX10 in early embryonic and fetal development. SOX10 is found in neural crest cells that form melanocytes,...
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Updated: Feb 27, 2026

Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes
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Modulating Wnt Signaling Rescues Palate Morphogenesis in Pax9 Mutant Mice.

C Li1, Y Lan1,2, R Krumlauf3,4

  • 11 Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Journal of Dental Research
|July 11, 2017
PubMed
Summary
This summary is machine-generated.

Canonical Wnt signaling is crucial for palate development, acting downstream of Pax9. Inhibiting Wnt antagonists like Dickkopf (DKK) and Wise partially rescued cleft palate in Pax9-deficient embryos.

Keywords:
Sostdc1Wnt antagonistcell signalingcleft palatecraniofacial biologytranscription factors

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Cleft palate is a common birth defect impacting embryonic development.
  • Wnt signaling pathway mutations are linked to cleft lip and palate.
  • The precise role of canonical Wnt signaling in secondary palate development remains unclear.

Purpose of the Study:

  • To investigate the role of canonical Wnt signaling in Pax9-mediated secondary palate development.
  • To elucidate the mechanisms by which Pax9 regulates palate morphogenesis via Wnt signaling.

Main Methods:

  • Analysis of gene expression (Axin2, Dkk2, β-catenin) in Pax9-deficient embryos.
  • Pharmacological inhibition of Dickkopf (DKK) activity in utero.
  • Genetic inactivation of Wise (a Wnt antagonist) in Pax9-deficient mice.
  • Assessment of palatal shelf elevation, reorientation, and hyaluronic acid accumulation.

Main Results:

  • Pax9 deficiency led to reduced Axin2 expression and decreased active β-catenin in posterior palatal shelves.
  • Increased Dkk2 expression was observed in Pax9-deficient embryos.
  • Inhibition of DKK activity and genetic inactivation of Wise partially rescued palate development in Pax9-deficient embryos.
  • Double mutants (Pax9del/del;Wise-/-) showed rescued palatal shelf elevation and hyaluronic acid accumulation.

Conclusions:

  • Canonical Wnt signaling is essential for secondary palate development.
  • Pax9 regulates palate morphogenesis by controlling canonical Wnt signaling.
  • Wnt antagonists, Dkk2 and Wise, play a significant role in this process.