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Updated: Jun 4, 2025
07:13
Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes
Published on: February 13, 2021
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Transcriptional factor ISL1 regulates palate development by tuning the SHH cascade
Chujing Zhang1, Yuting Zheng1, Yaping Qu1
1Zhejiang Key Laboratory of Organ Development and Regeneration, Institute of Developmental and Regenerative Biology, College of Life and Environmental Sciences, Hangzhou Normal University, China.
The FEBS Journal
|December 20, 2024
Summary
Ablation of Isl1 in developing palate epithelium causes cleft palate by disrupting mesenchymal cell proliferation and Shh signaling. Hedgehog signaling pathway modulation rescues these defects, highlighting Isl1
Area of Science:
- Developmental biology
- Genetics
- Craniofacial development
Background:
- Cleft palate is a common birth defect.
- Palate development relies on epithelial-mesenchymal interactions.
Purpose of the Study:
- Investigate the role of Isl1 in palate morphogenesis.
- Determine Isl1's mechanism in epithelial-mesenchymal communication.
Main Methods:
- Utilized Isl1 conditional knockout mouse models (Isl1Pitx2Cre).
- Analyzed palate development, cell proliferation, apoptosis, and gene expression (Shh, Sox2, Foxe1, Foxd2, Msx1).
- Employed transgenic rescue experiments (Tg-pmes-Ihh) to assess Hedgehog signaling pathway involvement.
Main Results:
- Isl1 ablation in oral epithelium resulted in complete cleft palate.
- Mesenchymal cell proliferation significantly decreased in mutant embryos.
- Downregulation of Shh and other developmental genes observed; ISL1 directly regulates Shh.
- Hedgehog signaling pathway activation rescued cleft palate defects.
Conclusions:
- ISL1 is crucial for palatal shelf morphogenesis.
- Isl1 regulates epithelial-mesenchymal communication through SHH signaling.
- Targeting Isl1 and SHH signaling offers potential therapeutic avenues for cleft palate.
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