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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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Updated: Nov 8, 2025

Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy
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A Highly Conserved Shh Enhancer Coordinates Hypothalamic and Craniofacial Development.

Zoe Crane-Smith1, Jeffrey Schoenebeck2, Katy A Graham1

  • 1Medical Research Council Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.

Frontiers in Cell and Developmental Biology
|April 19, 2021
PubMed
Summary
This summary is machine-generated.

The Shh brain enhancer 2 (SBE2) is crucial for proper embryonic brain development, particularly the hypothalamus. Its deletion disrupts Shh expression, impacting brain and craniofacial formation.

Keywords:
Shhcraniofacial formationembryonic developmentenhancerhypothalamic development

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Area of Science:

  • Developmental Biology
  • Evolutionary Biology
  • Genetics

Background:

  • Conserved enhancers regulate fundamental traits across species.
  • The Sonic Hedgehog (Shh) gene plays a vital role in embryonic development.
  • Understanding enhancer function is key to deciphering developmental processes.

Purpose of the Study:

  • To investigate the role of the Shh enhancer SBE2 in embryonic brain development.
  • To determine the impact of SBE2 deletion on Shh expression levels and downstream effects.
  • To elucidate the specific contributions of SBE2 to hypothalamic and craniofacial morphogenesis.

Main Methods:

  • Utilized mouse models with targeted deletion of the Shh enhancer SBE2.
  • Analyzed Shh expression patterns in the embryonic brain.
  • Examined anatomical phenotypes and gene expression related to brain and craniofacial development.
  • Created genetic crosses between SBE2 deletion and Shh null alleles.

Main Results:

  • SBE2 deletion significantly reduced Shh expression in the rostral diencephalon but caused no initial anatomical defects.
  • A secondary enhancer compensates for low Shh levels, mediating minimal expression.
  • Combined SBE2 deletion with Shh null allele disrupted brain and craniofacial development.
  • Shh expression levels critically influence dorsal-ventral patterning and neuronal induction in the hypothalamus.
  • Low Shh levels also affected the mediolateral patterning of cranial floor and viscerocranium bones.

Conclusions:

  • SBE2 is essential for elevating Shh expression to necessary levels for hypothalamic morphogenesis.
  • SBE2 ensures regional-specific Shh activity, critical for proper brain and craniofacial development.
  • This study reveals a novel morphogenic context for Shh, highlighting its sensitivity to expression levels in DV patterning and coordination with cranial bone formation.