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Updated: Feb 15, 2026
06:33
Probing the Roles of Physical Forces in Early Chick Embryonic Morphogenesis
Published on: June 5, 2018
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P63 expression plays a role in developmental rate, embryo size, and local morphogenesis
Julia C Boughner1, Matthijs C van Eede2, Shoshana Spring2
1Department of Anatomy & Cell Biology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Summary
The p63 gene is crucial for prenatal development. Loss of p63 causes developmental delays and malformations in mouse embryos, impacting organogenesis and overall growth.
Area of Science:
- Developmental Biology
- Genetics
- Morphogenesis
Background:
- The p63 gene plays a vital role in the development of various organs, including limbs, palate, teeth, and the urogenital tract.
- Altered p63 expression can disrupt developmental rates, leading to abnormal morphogenesis.
- This study aimed to validate a new embryo phenotyping software by assessing developmental delay in p63 knockout (p63-/-) mouse mutants.
Purpose of the Study:
- To validate a novel, unbiased embryo phenotyping software tool.
- To investigate whether developmental delay contributes to the pathological phenotype observed in p63-/- mouse embryos.
- To quantify dysmorphology and assess growth delay in p63-/- embryos compared to wild-type (WT) littermates.
Main Methods:
- Micro-computed tomography (micro-CT) scanning of fixed p63-/- embryos (n=6) at embryonic day (E) 15.5.
- Quantitative analysis using a digital WT atlas to determine volumetric differences between p63-/- and WT embryos.
- Assessment of malformations in epithelial derivatives and overall growth delay.
Main Results:
- p63-/- embryos exhibited a significant growth delay of approximately 22 hours (0.9 days) compared to WT embryos.
- At E15.5, mutant embryos showed overall size comparable to WT E14.6 but shape resembling WT E14.0.
- The phenotyping software identified malformations in epithelial derivatives, including limbs, tail, urogenital structures, brain, face, and teeth in p63-/- embryos.
Conclusions:
- The software atlas technique effectively characterized the p63-/- phenotype as a combination of developmental delay (heterochrony) and malformation (pathological shape/failed organogenesis).
- This research provides the first evidence for both global and local roles of p63 in prenatal growth and development.
- The findings highlight the critical function of p63 in normal embryonic development and morphogenesis.
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