Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 112, Issue 22, Pages 6800-6806Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1411269112
Keywords
non-CpG methylation; hydroxymethylation; MeCP2; Rett syndrome
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Funding
- Rett Syndrome Research Trust
- National Institutes of Health (NIH) [1R01NS048276]
- William Randolph Hearst fund
- NIH [T32GM007753]
- Howard Hughes Medical Institute Gilliam Fellowship
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DNA methylation at CpG dinucleotides is an important epigenetic regulator common to virtually all mammalian cell types, but recent evidence indicates that during early postnatal development neuronal genomes also accumulate uniquely high levels of two alternative forms of methylation, non-CpG methylation and hydroxymethylation. Here we discuss the distinct landscape of DNA methylation in neurons, how it is established, and how it might affect the binding and function of protein readers of DNA methylation. We review studies of one critical reader of DNA methylation in the brain, the Rett syndrome protein methyl CpG-binding protein 2 (MeCP2), and discuss how differential binding affinity of MeCP2 for non-CpG and hydroxymethylation may affect the function of this methyl-binding protein in the nervous system.
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