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首页> 外文期刊>Biochemical and Biophysical Research Communications >Absence of mitochondrial DNA methylation in mouse oocyte maturation, aging and early embryo development
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Absence of mitochondrial DNA methylation in mouse oocyte maturation, aging and early embryo development

机译：小鼠卵母细胞成熟，老化和早期胚胎发育中没有线粒体DNA甲基化

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摘要

Mitochondrial DNA (mtDNA) is important for oxidative phosphorylation; dysfunctions can play a role in many mitochondrial diseases and can also affect the aging of cells and individuals. DNA methylation is an important epigenetic modification that plays a critical role in regulating gene expression. While recent studies have revealed the existence of mtDNA methylation there are still controversies about mtDNA methylation due to the special structure of mtDNA. Mitochondria and DNA methylation are both essential for regulating oocyte maturation and early embryo development, but whether mtDNA methylation changes during this process is unknown. By employing bisulfite sequencing, we found that in the process of mouse oocyte maturation, postovulatory oocyte aging, and early embryo development, all analyzed mitochondrial genes, including 16S-CpGI, DCR, ND6, US, and ATP8, lacked 5'mC. Thus, mtDNA methylation does not occur in the oocyte and early embryo.
机译：线粒体DNA（MTDNA）对于氧化磷酸化是重要的; 功能障碍可以在许多线粒体疾病中发挥作用，并且还可以影响细胞和个体的老化。 DNA甲基化是一种重要的表观遗传改性，其在调节基因表达中起着关键作用。 虽然最近的研究表明，由于MTDNA的特殊结构，MTDNA甲基化的存在仍然存在关于MTDNA甲基化的争论。 线粒体和DNA甲基化对于调节卵母细胞成熟和早期胚胎发育至关重要，但在此过程中MTDNA甲基化变化是未知的。 通过使用亚硫酸氢盐测序，我们发现在小鼠卵母细胞成熟，后卵母细胞衰老和早期胚胎发育过程中，所有分析的线粒体基因，包括16S-CpGI，DCR，ND6，US和ATP8缺乏5'MC。 因此，在卵母细胞和早期胚胎中不会发生MTDNA甲基化。

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