Promoting cell proliferation or inhibiting DNSMT1 expression can effectively induce passive DNA de methylation.

DNA methylation is one of the most important ephegenological modifications of cytosine methylation, and many biological processes involve the regulation of DNA methylation level.
recently, Zheng Hui of the Guangzhou Institute of Biomedicine and Health of the Chinese Academy of Sciences discovered the new role of passive decethylation of DNA by studying the regulation of DNA methylation (methylation of cytosine) during cell proliferation.
the study was published online in Journal of Biological Chemistry.
DNA that is mediated by TET family proteins is considered actively to methylation.
newly synthesized sub-strands of DNA in the process of replication are not DNA methylation and need to be inherited by DNMT1 from the mother chain to the sub-chain during the S phase of the cell cycle.
this methylation genetic process can generally guarantee the stable inheritance of DNA methylation in the cell proliferation process.
if this process is impeded, DNA methylation levels will be significantly reduced, leading to passive methylation of DNA.
Zheng Hui's team found that the methylation of DNA during cell proliferation is mainly done by DNMT1 in the cell cycle S phase, but the work of DNMT1 in the S phase is not perfect, it still needs to continue in the cell cycle G2/M stage and G1 stage to complete.
this demand is more pronounced when cell proliferation accelerates or DNSMT1 expression is inhibited, resulting in the cell's overall DNA methylation level significantly higher in G1 than in G2/M.
genome-wide methylation sequencing suggests that such gaps are more focused on genes with high expression of pluripotent stem cell specificity.
therefore, when passive group DNA medehylation occurs, these genes become more powerful than methylation. Further research by the
team found that promoting cell proliferation or inhibiting DNSMT1 expression can effectively induce passive DNA de methylation and induce stronger de-methylation of plucular genes (Oct4, Nanog, etc.), thus further promoting somatic cell reprogramming.
study of the group has found that the efficiency of somatic cell reprogramming is positively related to the number of cell cycles rather than the time of reprogramming.
suggests that the mechanism may be that each cell cycle in the reprogramming process is equivalent to inducing decethylation on some erythrogenic genes.
the study was supported by the National Natural Science Foundation of China and the Guangdong Natural Science Foundation.
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