Absence of mitochondrial DNA methylation in mouse oocyte maturation, aging and early embryo development

Biochem Biophys Res Commun. 2019 Jun 11;513(4):912-918. doi: 10.1016/j.bbrc.2019.04.100. Epub 2019 Apr 17.

Abstract

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, 12S, and ATP8, lacked 5'mC. Thus, mtDNA methylation does not occur in the oocyte and early embryo.

Keywords: Aging; Early embryo development; Oocyte maturation; mtDNA methylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • DNA Methylation*
  • DNA, Mitochondrial / metabolism*
  • Embryo, Mammalian
  • Embryonic Development*
  • Epigenesis, Genetic
  • Mice
  • Oocytes / cytology*
  • Oocytes / metabolism

Substances

  • DNA, Mitochondrial