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Updated: Jun 1, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
Published on: April 1, 2022
Tgf-beta-mediated FasL-Fas-Caspase pathway is crucial during palatogenesis
1Department of Stomatology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
Abstract:
Programmed cell death, or apoptosis, is one of the fates of the medial edge epithelium (MEE) during palatal fusion. Transforming growth factor β (Tgf-β) signaling (such as Tgf-β3) is required for the disappearance of the MEE, but the relationship between Tgf-β3 and apoptosis remains unclear. Here we show that the Fas ligand (FasL)-Fas-Caspase extrinsic apoptosis pathway functions during palatal fusion in wild-type mice, but is not detectable in mice lacking Tgf-β3 (Tgf-β3 (-/-) ) or Tgfβr2 in the MEE (K14-Cre;Tgfbr2 (fl/fl)). Inhibition of the FasL-Fas system results in persistence of the midline epithelial seam (MES) and inhibition of caspase activity during palatal organ culture. Moreover, ectopic FasL protein induces apoptosis in MES of K14-Cre;Tgfbr2 (fl/fl) mice. Thus, we conclude that the FasL-Fas-caspase extrinsic apoptosis pathway is regulated by the Tgf-β3 signaling cascade and is essential for palatal fusion during craniofacial development.
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