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首页> 外文期刊>Cell cycle >Early demethylation of non-CpG, CpC-rich, elements in the myogenin 5'-flanking region: a priming effect on the spreading of active demethylation.
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Early demethylation of non-CpG, CpC-rich, elements in the myogenin 5'-flanking region: a priming effect on the spreading of active demethylation.

机译：肌原蛋白5'侧翼区域中富含CpC的非CpG元素的早期脱甲基作用：对活性脱甲基作用扩散的引发作用。

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摘要

The dynamic changes and structural patterns of DNA methylation of genes without CpG islands are poorly characterized. The relevance of CpG to the non-CpG methylation equilibrium in transcriptional repression is unknown. In this work, we analyzed the DNA methylation pattern of the 5'-flanking of the myogenin gene, a positive regulator of muscle differentiation with no CpG island and low CpG density, in both C2C12 muscle satellite cells and embryonic muscle. Embryonic brain was studied as a non-expressing tissue. High levels of both CpG and non-CpG methylation were observed in non-expressing experimental conditions. Both CpG and non-CpG methylation rapidly dropped during muscle differentiation and myogenin transcriptional activation, with an active demethylation dynamics. Non-CpG demethylation occurred more rapidly than CpG demethylation. Demethylation spread from initially highly methylated short CpC-rich elements to a virtually unmethylated status. These short elements have a high CpC content and density, share some motifs and largely coincide with putative recognition sequences of some differentiation-related transcription factors. Our findings point to a dynamically controlled equilibrium between CpG and non-CpG active demethylation in the transcriptional control of tissue-specific genes. The short CpC-rich elements are new structural features of the methylation machinery, whose functions may include priming the complete demethylation of a transcriptionally crucial DNA region.
机译：没有CpG岛的基因的DNA甲基化的动态变化和结构模式表征不佳。在转录抑制中，CpG与非CpG甲基化平衡的相关性尚不清楚。在这项工作中，我们分析了C2C12肌肉卫星细胞和胚胎肌肉中肌生成素基因5'侧翼的DNA甲基化模式，肌生成素基因是无CpG岛和低CpG密度的肌肉分化的正调节剂。胚胎脑被作为一种非表达组织进行了研究。在非表达实验条件下观察到高水平的CpG和非CpG甲基化。 CpG和非CpG甲基化在肌肉分化和肌生成素转录激活过程中迅速下降，并具有活跃的去甲基化动力学。非CpG脱甲基比CpG脱甲基更快。去甲基化从最初高度甲基化的富含CpC的短元素扩展到几乎未甲基化的状态。这些短元件具有较高的CpC含量和密度，共有一些基序，并且与某些分化相关转录因子的推定识别序列基本吻合。我们的发现指出在组织特异性基因的转录控制中，CpG和非CpG主动去甲基化之间的动态平衡控制。富含CpC的短元件是甲基化机制的新结构特征，其功能可能包括引发转录关键DNA区域的完全脱甲基。

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