Related Experiment Video

Updated: Aug 6, 2026

Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes
07:13

Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes

Published on: February 13, 2021

Loss of p130Cas/Bcar1 impairs palatal mesenchymal expansion and causes cleft palate

Tao Han1, Jing Gao2, Wei Wu1

  • 1Laboratory of Molecular and Cellular Biochemistry, Division of Oral Biological Sciences, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.

Scientific Reports
|July 16, 2026
PubMed

Insights

p130Cas protein is crucial for proper palatal shelf growth during embryonic development. Its absence in palatal mesenchyme causes cleft palate by impairing cell proliferation and expansion.

Area of Science:

  • Developmental Biology
  • Genetics
  • Cell Biology

Background:

  • Cleft palate is a common congenital anomaly resulting from disrupted palatogenesis.
  • The role of p130Crk-associated substrate (p130Cas), also known as breast cancer anti-estrogen resistance 1 (BCAR1), in late embryonic development is unclear due to early lethality in global knockout models.

Purpose of the Study:

  • To investigate the specific role of p130Cas in palatal development using a tamoxifen-inducible conditional knockout mouse model.
  • To determine whether p130Cas function in the palatal mesenchyme is essential for normal secondary palatogenesis.

Main Methods:

  • Generation and analysis of tamoxifen-inducible conditional knockout mice with targeted deletion of p130Cas.
  • Assessment of palatal shelf development, including growth and fusion.
  • Evaluation of mesenchymal cell proliferation using Ki-67 immunostaining and EdU incorporation assays.
  • In vitro analysis of primary mouse embryonic palatal mesenchymal (MEPM) cells from p130Cas-deficient embryos.

Main Results:

  • Conditional deletion of p130Cas in mice led to cleft palate, characterized by impaired horizontal growth of palatal shelves.
  • p130Cas deficiency resulted in significantly reduced mesenchymal cell proliferation within the palatal shelves.
  • Primary MEPM cells lacking p130Cas showed impaired proliferation and migration in vitro.
  • Epithelial-specific deletion of p130Cas did not cause cleft palate, highlighting the mesenchymal role.

Conclusions:

  • p130Cas is a critical regulator of palatal mesenchymal expansion during secondary palatogenesis.
  • Impaired proliferative growth of the palatal mesenchyme due to p130Cas deficiency is the developmental basis for cleft palate in this model.
  • p130Cas plays an essential, mesenchymal-specific role in ensuring normal palatal development.

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