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Molecular and Cellular Biology, March 2004, p. 1968-1982, Vol. 24, No. 5
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.5.1968-1982.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

DNA Methylation May Restrict but Does Not Determine Differential Gene Expression at the Sgy/Tead2 Locus during Mouse Development

Kotaro J. Kaneko,1 Theo Rein,2 Zong-Sheng Guo,3 Keith Latham,4 and Melvin L. DePamphilis1*

National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-2753,1 Max Planck Institute of Psychiatry, Munich D-80804, Germany,2 The Cancer Institute and Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213,3 The Fels Institute for Cancer Research and Molecular Biology and Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 191404

Received 29 August 2003/ Accepted 21 November 2003

Soggy (Sgy) and Tead2, two closely linked genes with CpG islands, were coordinately expressed in mouse preimplantation embryos and embryonic stem (ES) cells but were differentially expressed in differentiated cells. Analysis of established cell lines revealed that Sgy gene expression could be fully repressed by methylation of the Sgy promoter and that DNA methylation acted synergistically with chromatin deacetylation. Differential gene expression correlated with differential DNA methylation, resulting in sharp transitions from methylated to unmethylated DNA at the open promoter in both normal cells and tissues, as well as in established cell lines. However, neither promoter was methylated in normal cells and tissues even when its transcripts were undetectable. Moreover, the Sgy promoter remained unmethylated as Sgy expression was repressed during ES cell differentiation. Therefore, DNA methylation was not the primary determinant of Sgy/Tead2 expression. Nevertheless, Sgy expression was consistently restricted to basal levels whenever downstream regulatory sequences were methylated, suggesting that DNA methylation restricts but does not regulate differential gene expression during mouse development.

* Corresponding author. Mailing address: National Institute of Child Health and Human Development, Building 6, Room 416, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892-2753. Phone: (301) 402-8234. Fax: (301) 480-9354. E-mail: depamphm{at}mail.nih.gov.

Molecular and Cellular Biology, March 2004, p. 1968-1982, Vol. 24, No. 5
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.5.1968-1982.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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