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Updated: May 16, 2026
Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes
Published on: February 13, 2021
Gene expression changes in the secondary palate and mandible of Prdm16(-/-) mice
Dennis R Warner1, Justin P Wells, Robert M Greene
1Birth Defects Center, University of Louisville, 501 South Preston Street, Suite 350, Louisville, KY 40202, USA.
Abstract:
Loss of Prdm16 expression in the mouse leads to a complete cleft of the secondary palate. We have now determined changes in gene expression in the secondary palates of Prdm16(-/-) fetuses in an attempt to reveal the mechanism(s) leading to the failure of palate closure in these mice. Defined pathway-based polymerase chain reaction arrays were used to analyze the expression of genes associated with the extracellular matrix and the transforming growth factor-β and bone morphogenetic protein signaling networks, perturbations of which can lead to palatal clefting. Loss of Prdm16 expression in the secondary palate leads to alterations in numerous genes within these groups, many of which have been linked to chondrogenesis and osteogenesis. The expression of several genes linked to bone development was significantly changed in the developing secondary palate. Analysis of gene expression in the mandibles of Prdm16(-/-) fetuses revealed similar alterations in the same gene set. These data suggest that one function of Prdm16 is the regulation of genes that play a role in the differentiation of mesenchymal cells into chondro-/osteocytes.
Insights
Loss of Prdm16 gene expression causes cleft palate in mice by altering key bone development genes. This suggests Prdm16 regulates mesenchymal cell differentiation into bone and cartilage cells.
Area of Science:
- Developmental Biology
- Genetics
- Molecular Biology
Background:
- Prdm16 gene is crucial for secondary palate development in mice.
- Loss of Prdm16 results in a complete cleft of the secondary palate.
Purpose of the Study:
- To investigate the molecular mechanisms underlying palatal clefting due to Prdm16 deficiency.
- To identify gene expression changes in Prdm16(-/-) mouse fetuses.
Main Methods:
- Utilized pathway-based polymerase chain reaction arrays.
- Analyzed gene expression in secondary palates and mandibles of Prdm16(-/-) fetuses.
- Focused on genes in extracellular matrix and TGF-β/BMP signaling pathways.
Main Results:
- Prdm16 loss altered numerous genes involved in chondrogenesis and osteogenesis.
- Significant changes in bone development-related gene expression were observed in the palate.
- Similar gene expression alterations were found in the mandibles of Prdm16(-/-) fetuses.
Conclusions:
- Prdm16 plays a regulatory role in genes essential for mesenchymal cell differentiation.
- Prdm16 is implicated in the development of chondrocytes and osteocytes.
- The findings provide insights into the genetic regulation of palate closure and bone development.
