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Published on: February 13, 2021
Epigenetic regulation of Sox4 during palate development
Ratnam S Seelan1, Partha Mukhopadhyay, Dennis R Warner
1University of Louisville, Birth Defects Center, Department of Molecular, Cellular & Craniofacial Biology, ULSD, 501 S. Preston St., Suite 350, Louisville, KY 40202, USA.
Insights
Sox4 gene expression in developing mouse palates is regulated by DNA methylation. This epigenetic control is crucial for palate development and may offer insights into the causes of palatal clefts.
Area of Science:
- Developmental Biology
- Epigenetics
- Genetics
Background:
- Secondary palate development is critical for preventing palatal clefts.
- Understanding the genetic and epigenetic factors influencing palate development is essential for identifying the etiology of palatal clefts.
- Sox4 was identified as a differentially expressed gene during murine palate development.
Purpose of the Study:
- To investigate whether differential expression of Sox4 in the developing murine palate is regulated by DNA methylation.
- To identify specific CpG residues and regions involved in the epigenetic regulation of Sox4 in the palate.
Main Methods:
- In situ hybridization to determine Sox4 expression patterns.
- CpG methylation profiling of the Sox4 upstream region.
- Transfection analysis using modified Sox4 plasmid constructs in murine embryonic maxillary mesenchymal cells.
Main Results:
- Sox4 expression was localized to specific regions of the developing palate, including medial edge epithelium and rugae.
- Methylation of the Sox4 upstream promoter region significantly reduced promoter activity.
- A differentially methylated region (DMR4) was identified, with CpGs 83 and 85 being key regulators of Sox4 expression.
Conclusions:
- Sox4 is epigenetically regulated by DNA methylation during palate development.
- This epigenetic regulation is likely involved in mediating palatal fusion, extension, and rugae maintenance.
- Findings contribute to understanding the molecular mechanisms underlying palatal development and potential causes of palatal clefts.
Aim:
Identification of genes that contribute to secondary palate development provide a better understanding of the etiology of palatal clefts. Gene-expression profiling of the murine palate from gestational days 12-14 (GD12-14), a critical period in palate development, identified Sox4 as a differentially expressed gene. In this study, we have examined if the differential expression of Sox4 in the palate is due to changes in DNA methylation.
Materials & Methods:
In situ hybridization analysis was used to localize the expression of Sox4 in the developing murine secondary palate. CpG methylation profiling of a 1.8-kb upstream region of Sox4 in the secondary palate from GD12-14 and transfection analysis in murine embryonic maxillary mesenchymal cells using Sox4 deletion, mutant and in vitro methylated plasmid constructs were used to identify critical CpG residues regulating Sox4 expression in the palate.
Results:
Spatiotemporal analysis revealed that Sox4 is expressed in the medial edge epithelium and presumptive rugae-forming regions of the palate from GD12 to GD13. Following palatal shelf fusion on GD14, Sox4 was expressed exclusively in the epithelia of the palatal rugae, structures that serve as signaling centers for the anteroposterior extension of the palate, and that are thought to serve as neural stem cell niches. Methylation of a 1.8-kb region upstream of Sox4, containing the putative promoter, completely eliminated promoter activity. CpG methylation profiling of the 1.8-kb region identified a CpG-poor region (DMR4) that exhibited significant differential methylation during palate development, consistent with changes in Sox4 mRNA expression. Changes in the methylation of DMR4 were attributed primarily to CpGs 83 and 85.
Conclusion:
Our studies indicate that Sox4 is an epigenetically regulated gene that likely integrates multiple signaling systems for mediating palatal fusion, palatal extension and/or the maintenance of the neural stem cell niche in the rugae.
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