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Updated: May 12, 2026
08:26
A Quantitative Cell Migration Assay for Murine Enteric Neural Progenitors
Published on: September 18, 2013
Sox10 and Itgb1 interaction in enteric neural crest cell migration
Yuli Watanabe1, Florence Broders-Bondon, Viviane Baral
1INSERM U955, Equipe 11, F-94000 Créteil, France; Université Paris-Est, UMR_S955, UPEC, F-94000 Créteil, France.
Developmental Biology
|April 24, 2013
Summary
SOX10 is crucial for enteric nervous system development by regulating enteric neural crest cell migration and interaction with β1-integrins, impacting Hirschsprung disease.
Area of Science:
- Developmental Biology
- Neuroscience
- Genetics
Background:
- SOX10 is a key transcription factor in enteric nervous system (ENS) development.
- SOX10 mutations are linked to syndromic Hirschsprung disease (HSCR).
- The precise role of SOX10 in enteric neural crest cell (ENCC) migration and adhesion is not fully understood.
Purpose of the Study:
- To investigate the role of SOX10 in ENCC migration and its interaction with β1-integrins during ENS development.
- To elucidate the molecular mechanisms underlying ENS defects in SOX10-related disorders.
Main Methods:
- Generation of double mutant mice (Sox10(lacZ/+); Ht-PA::Cre; beta1(neo/fl)) to study gene interactions.
- Phenotypic analysis of ENS development in mutant embryos using microscopy.
- Video-microscopy to assess ENCC migration speed and directionality.
- Analysis of β1-integrin expression in response to SOX10 modulation.
Main Results:
- Double mutant embryos exhibited more severe intestinal aganglionosis and neuronal disorganization than single mutants.
- Defects in ENS development were observed early (E11.5) and persisted postnatally.
- Reduced ENCC migration speed and altered directionality were identified as key defects.
- SOX10 modulation affected β1-integrin expression, indicating SOX10's role in regulating this adhesion molecule.
Conclusions:
- SOX10 plays a critical role in regulating ENCC adhesion and migration through interaction with β1-integrins.
- A balanced interaction between SOX10 and β1-integrins is essential for normal ENS development.
- These findings contribute to understanding the cellular and molecular basis of HSCR and other ENS defects associated with SOX10 mutations.
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