Tandem B1 Elements Located in a Mouse Methylation Center Provide a Target for de Novo DNA Methylation

• Published in: The Journal of biological chemistry Vol. 274; no. 51; pp. 36357 - 36361
• Main Authors: Yates, P A, Burman, R W, Mummaneni, P, Krussel, S, Turker, M S
• Format: Journal Article
• Language: English
• Published: United States American Society for Biochemistry and Molecular Biology 17-12-1999
• Subjects: Animals; Base Sequence; DNA - genetics; DNA - metabolism; DNA Methylation; DNA methyltransferase; Mice; Molecular Sequence Data; Repetitive Sequences, Nucleic Acid; Sequence Analysis, DNA
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1074/jbc.274.51.36357

A cis-acting methylation center that signals de novo DNA methylation is located upstream of the mouse Aprt gene. In the current study, two approaches were taken to determine if tandem B1 repetitive elements found at the 3′ end of
the methylation center contribute to the methylation signal. First, bisulfite genomic sequencing demonstrated that CpG sites
within the B1 elements were methylated at relative levels of 43% in embryonal stem cells deficient for the maintenance DNA
methyltransferase when compared with wild type embryonal stem cells. Second, the ability of the B1 elements to signal de novo methylation upon stable transfection into mouse embryonal carcinoma cells was examined. This approach demonstrated that the
B1 elements were methylated de novo to a high level in the embryonal carcinoma cells and that the B1 elements acted synergistically. The results from these experiments
provide strong evidence that the tandem B1 repetitive elements provide a significant fraction of the methylation center signal.
By extension, they also support the hypothesis that one role for DNA methylation in mammals is to protect the genome from
expression and transposition of parasitic elements.