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Related Experiment Video

Updated: Dec 29, 2025

Immunostaining to Visualize Murine Enteric Nervous System Development
07:54

Immunostaining to Visualize Murine Enteric Nervous System Development

Published on: April 29, 2015

11.9K

Dlx1/2 mice have abnormal enteric nervous system function.

Christina M Wright1,2, James P Garifallou3,2, Sabine Schneider1,2

  • 1Department of Pediatrics.

JCI Insight
|February 5, 2020
PubMed
Summary
This summary is machine-generated.

Mice lacking DLX1 and DLX2 transcription factors exhibit bowel motility issues due to reduced VIP-expressing neurons, even without structural defects in the enteric nervous system (ENS). This highlights a new link between DLX genes and VIP, relevant to motility disorders.

Keywords:
DevelopmentEmbryonic developmentNeurodevelopmentNeuroscienceTranscription

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Gastroenterology

Background:

  • DLX1 and DLX2 are transcription factors crucial for the enteric nervous system (ENS).
  • Previous studies noted potential bowel motility problems in mice lacking DLX1/2, but these were not fully understood.
  • The precise role of DLX1/2 in ENS function and motility remained unclear.

Purpose of the Study:

  • To investigate the functional consequences of DLX1/2 deficiency on small bowel motility.
  • To elucidate the underlying molecular mechanisms, particularly the role of vasoactive intestinal peptide (VIP).
  • To determine if structural ENS defects are present in DLX1/2 deficient mice.

Main Methods:

  • Comparative analysis of small bowel transit and motility in wild-type, Dlx1/2-/-, and Dlx1-/- mice.
  • Detailed anatomical studies of the ENS, including precursor migration and neuronal/glial density.
  • RNA sequencing of the ENS from Dlx1/2-/- mice to identify gene dysregulation.
  • Immunohistochemistry and reporter mice to assess VIP expression and VIP-lineage neurons.

Main Results:

  • Dlx1/2-/- mice displayed significantly slower small bowel transit and impaired neurally mediated contraction complexes.
  • No anatomical defects in ENS precursor migration or neuronal/glial density were observed in Dlx1/2-/- or Dlx1-/- mice.
  • RNA sequencing revealed dysregulation of genes including VIP in Dlx1/2-/- ENS; confirmed by reduced VIP expression and fewer VIP-lineage neurons.

Conclusions:

  • DLX1/2 transcription factors are essential for normal small bowel motility, independent of gross ENS structural defects.
  • A novel link exists between DLX genes and the regulation of VIP expression and VIP-neuron development in the ENS.
  • These findings offer insights into motility disorders like chronic intestinal pseudo-obstruction (CIPO).