Methylated DNA attracts methylated DNA binding proteins, which recruit a cluster of proteins referred to as repressor complexes, which include histone deacetylases that result in inactive chromatin and the silencing of gene expression.105,106 The model positioning DNA methylation as driving chromatin inactivation is pervasive. Nevertheless, new data suggest that the state of chromatin structure can also determine DNA methylation and that chromatin can affect DNA methylation in both directions triggering either de novo DNA methylation or demethylation.107-109 These data revise the classic model of a DNA methylation pattern that is determined during development and maintained through life, and adopt a more dynamic view of the DNA methylation pattern as an interface between the dynamic environment and the static genome. Thus, although DNA methylation is an extremely stable signal, it can be altered later in life when there is a sufficiently stable and consistent signal to activate the chromatin. Transient changes in cellular function and chromatin structure are not accompanied by changes in DNA methylation. The relation between chromatin state and DNA methylation forms a molecular link through which environmental signals
