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Published on: October 1, 2007
Stage specific requirement of platelet-derived growth factor receptor-α in embryonic development
Chen Qian1, Carol Wing Yan Wong1, Zhongluan Wu1
1Department of Surgery, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
Insights
Altering Platelet-Derived Growth Factor Receptor Alpha (PDGFRα) expression during mouse embryonic development causes skeletal and abdominal wall defects. The timing of PDGFRα deletion impacts the severity and type of congenital anomalies observed.
Area of Science:
- Developmental Biology
- Genetics
- Molecular Biology
Background:
- Platelet-derived growth factor receptor alpha (PDGFRα) is essential for embryonic development.
- PDGFRα signaling is critical for the proper formation of multiple embryonic structures.
- Previous studies indicated PDGFRα deletion leads to complex developmental defects, but temporal requirements were unclear.
Purpose of the Study:
- To investigate the temporal requirements of PDGFRα during embryonic development.
- To determine if the timing of PDGFRα deletion influences specific developmental anomalies.
Main Methods:
- Conditional deletion of Pdgfra in Pdgfra-expressing tissues at various embryonic stages (E7.5-E10.5) in mice.
- Examination and quantification of resulting developmental anomalies in embryos.
- Analysis of apoptosis in Pdgfra-expressing tissues following deletion.
Main Results:
- Conditional Pdgfra deletion at different embryonic stages resulted in orofacial cleft, spina bifida, rib cage deformities, and omphalocele.
- The specific day of Pdgfra deletion influenced the incidence, severity, and combination of these anomalies.
- Pdgfra deletion led to apoptosis of relevant tissues and subsequent developmental defects in their derivatives.
Conclusions:
- Conditional Pdgfra knockout embryos exhibit phenotypes resembling common human congenital anomalies like orofacial cleft, spina bifida, and omphalocele.
- Dysregulated PDGFRA expression is a potential cause of these congenital anomalies in humans.
- Further research should focus on identifying regulatory elements of human PDGFRA and investigating their role in congenital defects.
Background:
Platelet-derived growth factor receptor alpha (PDGFRα) is a cell-surface receptor tyrosine kinase for platelet-derived growth factors. Correct timing and level of Pdgfra expression is crucial for embryo development, and deletion of Pdgfra caused developmental defects of multiple endoderm and mesoderm derived structures, resulting in a complex phenotypes including orofacial cleft, spina bifida, rib deformities, and omphalocele in mice. However, it is not clear if deletion of Pdgfra at different embryonic stages differentially affects these structures.
Purpose:
To address the temporal requirement of Pdgfra in embryonic development.
Methods:
We have deleted the Pdgfra in Pdgfra-expressing tissues at different embryonic stages in mice, examined and quantified the developmental anomalies.
Results:
Current study showed that (i) conditional deletion of Pdgfra at different embryonic days (between E7.5 and E10.5) resulted in orofacial cleft, spina bifida, rib cage deformities, and omphalocele, and (ii) the day of Pdgfra deletion influenced the combinations, incidence and severities of these anomalies. Deletion of Pdgfra caused apoptosis of Pdgfra-expressing tissues, and developmental defects of their derivatives.
Conclusion:
Orofacial cleft, spina bifida and omphalocele are among the commonest skeletal and abdominal wall defects of newborns, but their genetic etiologies are largely unknown. The remarkable resemblance of our conditional Pdgfra knockout embryos to theses human congenital anomalies, suggesting that dysregulated PDGFRA expression could cause these anomalies in human. Future work should aim at defining (a) the regulatory elements for the expression of the human PDGFRA during embryonic development, and (b) if mutations / sequence variations of these regulatory elements cause these anomalies.
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