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Molecular and Cellular Biology, November 2001, p. 7601-7606, Vol. 21, No. 22
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.22.7601-7606.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

CpG Binding Protein Is Crucial for Early Embryonic Development

Diana L. Carlone and David G. Skalnik*

Herman B Wells Center for Pediatric Research, Section of Pediatric Hematology/Oncology, Department of Pediatrics, and Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202

Received 31 July 2001/Accepted 28 August 2001

Epigenetic modification of DNA via CpG methylation is essential for the proper regulation of gene expression during embryonic development. Methylation of CpG motifs results in gene repression, while CpG island-containing genes are maintained in an unmethylated state and are transcriptionally active. The molecular mechanisms involved in maintaining the hypomethylation of CpG islands remain unclear. The transcriptional activator CpG binding protein (CGBP) exhibits a unique binding specificity for DNA elements that contain unmethylated CpG motifs, which makes it a potential candidate for the regulation of CpG island-containing genes. In order to assess the global function of this protein, mice lacking CGBP were generated via homologous recombination. No viable mutant mice were identified, indicating that CGBP is required for murine development. Mutant embryos were also absent between 6.5 and 12.5 days postcoitum (dpc). Approximately, one-fourth of all implantation sites at 6.5 dpc appeared empty with no intact embryos present. However, histological examination of 6.5-dpc implantation sites revealed the presence of embryo remnants, indicating that CGBP mutant embryos die very early in development. In vitro blastocyst outgrowth assays revealed that CGBP-null blastocysts are viable and capable of hatching and forming both an inner cell mass and a trophectoderm. Therefore, CGBP plays a crucial role in embryo viability and peri-implantation development.

* Corresponding author. Mailing address: Herman B Wells Center for Pediatric Research, Cancer Research Building, Room 472, Indiana University School of Medicine, 1044 West Walnut St., Indianapolis, IN 46202. Phone: (317) 274-8977. Fax: (317) 274-8928. E-mail: dskalnik{at}iupui.edu.

Molecular and Cellular Biology, November 2001, p. 7601-7606, Vol. 21, No. 22
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.22.7601-7606.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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