DNA methylation is one of the most important epigenetic modifications of cytosine methylation, and many biological processes involve the regulation of DNA methylation levels. Recently, the Zheng Hui group of the Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences, discovered the new role of DNA passive demethylation by studying the regulation of DNA methylation (methylation of cytosine) during cell proliferation. Related research results are published online in the Journal of Biological Chemistry.
TET family protein-mediated DNA demethylation is considered to be active demethylation. The newly synthesized daughter strand of DNA during the process of replication is free of DNA methylation, and it is necessary to complete the inheritance of DNA methylation from the parental strand to the daughter strand by DNMT1 in the S phase of the cell cycle. This methylation genetic process generally ensures stable inheritance of DNA methylation during cell proliferation. If this process is hindered, the level of DNA methylation will be significantly reduced, leading to passive demethylation of DNA.
Zheng Hui's research team found that the methylation of DNA during cell proliferation is mainly completed by DNMT1 in the S phase of the cell cycle, but the work of DNMT1 in S phase is not perfect, and it still needs to continue G2 in the cell cycle. The /M period and the G1 period are completed. This requirement is more pronounced when cell proliferation is accelerated or DNMT1 expression is inhibited, resulting in a significantly higher overall DNA methylation level in the G1 phase than in the G2/M phase. Further genome-wide methylation sequencing revealed that such gaps are more concentrated on genes with high specific expression of pluripotent stem cells. Therefore, when demethylation of passive group DNA occurs, these genes undergo stronger demethylation. Further research by the research team found that promoting cell proliferation or inhibiting DNMT1 expression can effectively induce passive DNA demethylation and induce stronger demethylation of pluripotency genes (Oct4, Nanog, etc.), thereby further promoting somatic cell weight. program.
The level of DNA methylation in cells in the G1 phase is higher than in the G2/M phase. Passive DNA demethylation further increases such gaps and regulates downstream pathways.
Previous research by the research team has found that somatic cell reprogramming efficiency is positively correlated with the number of cell cycle occurrences rather than reprogramming. This study suggests that the mechanism may be that each cell cycle in the reprogramming process is equivalent to inducing demethylation on some pluripotency genes.
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