Epigenetic Regulation of Genomic Stability by Vitamin C.
Epigenetic Regulation of Genomic Stability by Vitamin C.
复制标题
维生素C对基因组稳定性的表观遗传调节。
DOI：
10.3389/fgene.2021.675780
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发表时间：
2021
影响因子：
3.7
通讯作者：
Cimmino L
中科院分区：
文献类型：
--
作者：
Brabson JP;Leesang T;Mohammad S;Cimmino L
DNA甲基化在维持基因组稳定性中起着重要作用。Ten-11易位蛋白（Ten-eleven translocation proteins，TCN）是一类铁离子和α-KG依赖性双加氧酶，通过氧化5-甲基胞嘧啶（5-methylcystosine，5 mC）生成5-羟甲基胞嘧啶（5-hydroxymethylcytosine，5 hmC）、5-甲酰基胞嘧啶（5-formylcytosine，5 fC）和5-羧基胞嘧啶（5-carboxylcytosine，5caC）来调节DNA甲基化水平。这些氧化的甲基胞嘧啶通过触发碱基切除修复和用未甲基化的胞嘧啶取代5 fC和5caC来促进DNA复制时的被动去甲基化或主动DNA去甲基化。过去十年的几项研究表明，泰特功能的丧失导致DNA超甲基化和基因组不稳定性增加。维生素C是泰特酶的辅因子，可增加5 hmC的形成并促进DNA去甲基化，这表明这种必需维生素除了具有抗氧化特性外，还可直接影响基因组稳定性。本文综述了DNA甲基化、泰特活性和维生素C在DNA甲基化和DNA修复之间的相互作用中的作用。
DNA methylation plays an important role in the maintenance of genomic stability. Ten-eleven translocation proteins (TETs) are a family of iron (Fe2+) and α-KG -dependent dioxygenases that regulate DNA methylation levels by oxidizing 5-methylcystosine (5mC) to generate 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC). These oxidized methylcytosines promote passive demethylation upon DNA replication, or active DNA demethylation, by triggering base excision repair and replacement of 5fC and 5caC with an unmethylated cytosine. Several studies over the last decade have shown that loss of TET function leads to DNA hypermethylation and increased genomic instability. Vitamin C, a cofactor of TET enzymes, increases 5hmC formation and promotes DNA demethylation, suggesting that this essential vitamin, in addition to its antioxidant properties, can also directly influence genomic stability. This review will highlight the functional role of DNA methylation, TET activity and vitamin C, in the crosstalk between DNA methylation and DNA repair.
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