Institute of Biochemistry, Stuttgart University, Pfaffenwaldring 55, D-70569 Stuttgart, Germany.
Institute of Biochemistry, Stuttgart University, Pfaffenwaldring 55, D-70569 Stuttgart, Germany.
Trends Biochem Sci. 2014 Jul;39(7):310-8. doi: 10.1016/j.tibs.2014.05.002. Epub 2014 Jun 16.
The widely-cited model of maintenance of DNA methylation at CpG sites implies that DNA methylation is introduced by the Dnmt3 de novo DNA methyltransferases during early development, and methylation at hemimethylated CpG sites is specifically maintained by the Dnmt1 maintenance methyltransferase. However, substantial experimental evidence from the past decade indicates that this simple model needs to be revised. DNA methylation can be described by a dynamic stochastic model, in which DNA methylation at each site is determined by the local activity of DNA methyltransferases (Dnmts), DNA demethylases, and the DNA replication rate. Through the targeting and regulation of these enzymes, DNA methylation is controlled by the network of chromatin marks.
广泛引用的 CpG 位点 DNA 甲基化维持模型表明,DNA 甲基化是由 Dnmt3 从头 DNA 甲基转移酶在早期发育过程中引入的,而半甲基化 CpG 位点的甲基化则由 Dnmt1 维持甲基转移酶特异性维持。然而,过去十年的大量实验证据表明,这个简单的模型需要修正。DNA 甲基化可以用一个动态随机模型来描述,在这个模型中,每个位点的 DNA 甲基化由 DNA 甲基转移酶 (Dnmts)、DNA 去甲基酶和 DNA 复制率的局部活性决定。通过这些酶的靶向和调节,DNA 甲基化受染色质标记网络的控制。