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Updated: Sep 29, 2025

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
Published on: April 1, 2022
AP-2α and AP-2β cooperatively function in the craniofacial surface ectoderm to regulate chromatin and gene expression
Eric Van Otterloo1,2,3,4, Isaac Milanda4, Hamish Pike4
1Iowa Institute for Oral Health Research, College of Dentistry & Dental Clinics, University of Iowa, Iowa City, United States.
Loss of AP-2 transcription factors in embryonic ectoderm disrupts craniofacial development, causing clefts and jaw fusion. Restoring WNT signaling rescued these defects, highlighting AP-2
Area of Science:
- Developmental biology
- Genetics
- Craniofacial development
Background:
- Facial surface ectoderm is crucial for cranial neural crest development.
- Molecular mechanisms of ectodermal signaling are not fully understood.
Purpose of the Study:
- Investigate the role of AP-2 transcription factors in embryonic ectoderm.
- Elucidate the genetic programs governing craniofacial development.
Main Methods:
- Mouse models with targeted AP-2α and AP-2ß deletion in ectoderm.
- ATAC-seq and RNA-seq for chromatin accessibility and gene expression analysis.
- Wnt1 ligand overexpression for rescue experiments.
Main Results:
- AP-2 deficiency caused severe craniofacial abnormalities, including clefts and jaw fusion.
- Significant changes in chromatin accessibility and gene expression were observed.
- Loss of AP-2 impacted skin differentiation and WNT signaling pathways.
Conclusions:
- AP-2 transcription factors are essential for ectodermal signaling in craniofacial development.
- WNT pathway is a key target regulated by AP-2.
- Findings provide insights into the gene regulatory network controlling vertebrate craniofacial formation.
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