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. 2019 Feb 12;5:11. doi: 10.1038/s41421-018-0074-6

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — a Suppressing Dnmt1 with sh-Dnmt1 induces passive DNA demethylation by impairing the methylation of CpG sites on strand newly synthesized during the S phase. The over-expression of Tet1 induces active DNA demethylation by demethylating both hemi-methylated and full-methylated CpG sites. TET1 has higher abilities to demethylate hemi-methylated CpG sites than full-methylated CpG sites. b Both passive and active DNA demethylation were enriched at core pluripotency loci and promoted somatic cell reprogramming in the absence of Vc. Because of the higher abilities of active DNA demethylation than passive DNA demethylation to open the chromatin structure and regulate gene expression and the abilities of Vc to increase the demethylation activity of TET1, the over-expression of Tet1-induced demethylation genes that promoted the EMT, up-regulated these genes, and impaired reprogramming in the presence of Vc