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Véron, Nathalie Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
- The search for pathways removing DNA methylation
- Tet proteins: a new enzyme class modifying methylcytosine bases
- Tet proteins and hydroxymethylcytosine in development
- Functional roles in gene regulation
- Mechanistic models for transforming methylated bases
- Tet function in demethylation?
- Related Primary Literature
- Additional Reading
At the beginning of life, one single cell, the fertilized oocyte, has the capacity to generate all cell types of the body through cellular division and execution of differentiation programs. As the deoxyribonucleic acid (DNA) sequence in most of the cells of an organism is identical, cellular identity relies on the interpretation of genomic information. The driving force in this process is a correct spatiotemporal regulation of gene expression that prevents errors causing developmental failure and disease. Partly, this is controlled by cell-specific enzymatic modifications of chromatin, which is the tight association of acidic DNA and basic protein complexes (the histone-containing nucleosomes). Enzymes involved in the shaping of chromatin can, for example, posttranslationally modify amino acids of histones by adding methyl or acetyl groups. Furthermore, small proteins such as ubiquitin or small ubiquitin-like modifier (SUMO) proteins can be enzymatically coupled to histones, regulating the interpretation of the underlying genomic information. Other enzyme classes directly add functional groups to DNA bases. Various combinations of these so-called epigenetic modifications activate or repress gene expression and define a cell-specific genome function, which is heritable from one cell to another on cell division. Epigenetic configurations of cell types dynamically respond to environmental cues and vary among individuals, as has been shown for monozygotic twins (whose DNA sequences are nearly identical).
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