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Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
Published on: January 31, 2025
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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
Summary
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.
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.
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