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Sonic Hedgehog Signaling Is Required for Cyp26 Expression during Embryonic Development.

Maha El Shahawy1,2, Claes-Göran Reibring3, Kristina Hallberg4

  • 1Department of Oral Biochemistry, Sahlgrenska Academy at the University of Gothenburg, SE-40530 Göteborg, Sweden. maha.el.shahawy@odontologi.gu.se.

International Journal of Molecular Sciences
|May 11, 2019
PubMed
Summary
This summary is machine-generated.

Sonic hedgehog (SHH) signaling prevents abnormal retinoic acid activity during embryonic development. SHH loss-of-function causes developmental defects by allowing excessive retinoic acid signaling, impacting organogenesis.

Keywords:
CRE/LoxPCyp26 enzymescongenital anomalieshedgehog signalingmouse modelsretinoic acidsmoothenedsonic hedgehog

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Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • Signaling pathways are crucial for embryonic development and disease.
  • Hedgehog and retinoic acid pathways are key regulators of development.
  • Interactions between these pathways during organogenesis are largely unknown.

Purpose of the Study:

  • To investigate the interaction between Hedgehog and retinoic acid signaling during organogenesis.
  • To understand the role of Sonic hedgehog (SHH) in regulating retinoic acid signaling.
  • To elucidate the impact of pathway crosstalk on congenital malformations.

Main Methods:

  • Genetic manipulation in mouse models.
  • Experimental approaches to study signaling pathways.
  • Analysis of embryonic organ development (tail, genital tubercle, secondary palate).

Main Results:

  • SHH loss-of-function in mice phenocopied enhanced retinoic acid signaling.
  • SHH is essential for maintaining expression of Cyp26 genes, which regulate retinoic acid.
  • Disruptions in either pathway led to similar developmental defects in various organs.

Conclusions:

  • Hedgehog and retinoic acid pathways interact antagonistically during organogenesis.
  • SHH signaling acts as a critical brake on retinoic acid activity.
  • Precise calibration of both pathways is vital for normal tissue patterning and organ development.