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Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

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.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Notch Signaling Pathway03:14

Notch Signaling Pathway

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.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Determination01:51

Determination

During embryogenesis, cells become progressively committed to different fates through a two-step process: specification followed by determination. Specification is demonstrated by removing a segment of an early embryo, “neutrally” culturing the tissue in vitro—for example, in a petri dish with simple medium—and then observing the derivatives. If the cultured region gives rise to cell types that it would normally generate in the embryo, this means that it is specified. In contrast, determination...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

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.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

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Related Experiment Video

Updated: May 9, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

SP8 regulates signaling centers during craniofacial development.

Abigail D Kasberg1, Eric W Brunskill, S Steven Potter

  • 1Division of Developmental Biology, Cincinnati Children's Medical Center, Cincinnati, OH 45229, USA.

Developmental Biology
|July 23, 2013
PubMed
Summary

The Sp8 gene is crucial for craniofacial development, regulating neural crest cell survival and proliferation. Its mutation leads to severe facial malformations by disrupting FGF signaling in key developmental centers.

Keywords:
Anterior neural ridgeCraniofacial developmentCyclopamineFGF17FGF8Neural crestOlfactory pitsSP8Signaling center

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Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy

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Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development
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Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development

Published on: March 24, 2011

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Last Updated: May 9, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy
09:16

Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy

Published on: January 30, 2014

Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development
09:25

Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development

Published on: March 24, 2011

Area of Science:

  • Developmental Biology
  • Genetics
  • Craniofacial Development

Background:

  • Vertebrate facial structures develop from neural crest (NC) cells.
  • Signaling centers like the anterior neural ridge (ANR) and olfactory pit (OP) guide NC cell development via FGF.
  • The mechanisms maintaining these signaling centers remain unclear.

Purpose of the Study:

  • Investigate the role of the Sp8 gene in craniofacial development.
  • Determine how Sp8 influences signaling centers and NC cell behavior.
  • Identify downstream targets and rescue strategies for Sp8-related craniofacial defects.

Main Methods:

  • Analysis of Sp8 mutant mice exhibiting craniofacial malformations.
  • Conditional mutagenesis to assess Sp8 function in specific cell types.
  • Apoptosis and proliferation assays for NC cells.
  • Gene expression analysis using microarrays and in situ hybridization.
  • Genetic and pharmaceutical rescue experiments.

Main Results:

  • Sp8 mutants display severe facial underdevelopment, midline defects, and cranial bone loss.
  • Sp8 is essential in ANR and OP signaling centers, not directly in NC or mesoderm cells.
  • Sp8 deficiency increases NC cell apoptosis and reduces proliferation.
  • Sp8 regulates Fgf8 and Fgf17 expression in ANR and OP.
  • Sonic Hedgehog (SHH) signaling inhibition partially rescues the phenotype.

Conclusions:

  • Sp8 is critical for maintaining ANR and OP signaling centers during craniofacial development.
  • Sp8 promotes NC and paraxial mesoderm survival and proliferation by regulating FGF signaling.
  • Targeting SHH signaling offers a potential therapeutic avenue for Sp8-related craniofacial disorders.