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Related Experiment Video

Updated: Jun 17, 2026

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

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

Published on: February 13, 2021

Prdm16 is required for normal palatogenesis in mice.

Bryan C Bjork¹, Annick Turbe-Doan, Mary Prysak

¹Genetics Division, Brigham and Women's Hospital, Harvard Medical School, New Research Building, Boston, MA 02115, USA.

Human Molecular Genetics

|December 17, 2009

Summary

A novel mouse model reveals that mutations in the Prdm16 gene cause non-syndromic cleft palate by disrupting transforming growth factor beta signaling during embryonic development.

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Last Updated: Jun 17, 2026

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

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Published on: February 13, 2021

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Area of Science:

Developmental Biology
Genetics
Molecular Biology

Background:

Transcriptional cofactors regulate transforming growth factor beta (TGFbeta) superfamily signaling.
These cofactors are crucial for embryonic development, particularly craniofacial development.

Purpose of the Study:

To investigate the genetic basis of non-syndromic cleft palate (NSCP).
To characterize a new mouse model for cleft secondary palate (CSP).

Main Methods:

Generation of an N-ethyl-N-nitrosourea-induced mouse model (csp1).
Identification of an intronic Prdm16 splicing mutation as the causative agent.
Analysis of Prdm16 gene expression and its role in TGFbeta signaling.

Main Results:

The csp1 mouse model exhibits cleft secondary palate due to micrognathia and failed palate shelf elevation.
The mutation affects Prdm16, a transcriptional cofactor regulating TGFbeta signaling.
Prdm16 expression patterns correlate with its role in palate and craniofacial development.

Conclusions:

Prdm16 mutations are a potential cause of non-syndromic cleft palate in humans.
The identified mouse model mimics human Pierre Robin sequence (PRS)-like cleft palate.
PRDM16 is a candidate gene for mutations in human clefting disorders, including NSCP and PRS-like CP.