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The dinucleotide CG as a genomic signalling module

机译：二核苷酸CG作为基因组信号传导模块

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The DNA sequence 5’CG (CpG) is self-complementaryand can exist in three major chemical forms depending onthe modification status of its cytosine moiety. To understandthe functional significance of the CpG dinucleotide,we study proteins that bind either its methylated orunmethylated form. These proteins are likely mediators ofCpG signalling that influence chromatin modification andthereby genome activity. The local density of CpG variesdramatically within genomic DNA. In the bulk genomeCpG is rare and highly methylated, but in so-called “CpGislands” (CGIs) it is dense and usually non-methylated. Asignature histone mark at non-methylated CGIs and alsoat transcriptionally active genes is trimethylation of histoneH3 lysine 4. We are exploring the mechanisms bywhich DNA sequence features that are shared by all CGIsinfluence this and other epigenetic marks. In contrast, proteinsthat interact with methyl-CpG are thought to promotegene silencing by recruiting transcriptionalcorepressors. In particular mutations in the gene for themethyl-CpG binding protein MeCP2 cause the autismspectrum disorder Rett Syndrome. By studying MeCP2 weare learning about its partner proteins that mediate effectson chromatin. These findings allow us to evaluate competingmodels for MeCP2 function and they illuminate thebiology of DNA methylation and the molecular basis ofthis neurological condition.
机译：DNA序列5’CG（CpG）是自我互补的，可以根据其胞嘧啶部分的修饰状态以三种主要化学形式存在。为了了解CpG二核苷酸的功能意义，我们研究了结合其甲基化或未甲基化形式的蛋白质。这些蛋白质可能是CpG信号传导的介体，可影响染色质修饰并从而影响基因组活性。 CpG的局部密度在基因组DNA中急剧变化。在整个基因组中，CpG是罕见的并且高度甲基化，但是在所谓的“ CpGislands”（CGI）中，它是致密的，通常是非甲基化的。非甲基化CGI和转录活性基因上的签名组蛋白标记是组蛋白H3赖氨酸4的三甲基化。我们正在探索所有CGI共有的DNA序列特征影响该标记和其他表观遗传标记的机制。相比之下，与甲基CpG相互作用的蛋白质被认为可以通过募集转录共表达因子来促进基因沉默。特别地，甲基-CpG结合蛋白MeCP2的基因突变引起自闭症谱系障碍Rett综合征。通过研究磨损的MeCP2，了解其介导染色质效应的伴侣蛋白。这些发现使我们能够评估MeCP2功能的竞争模型，它们阐明了DNA甲基化的生物学和这种神经疾病的分子基础。

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