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. 2019 Aug 10;47(17):9053–9068. doi: 10.1093/nar/gkz626

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© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 7. — SET8 regulates global DNA methylation independent of DNMT3A/3B and suppresses DNA methylation in the G2/M phase of cell cycle. (A) Western blot analysis of DNMT3A/3B DKO HeLa cells showing that loss of DNMT3A and DNMT3B did not affect the levels of UHRF1 and DNMT1. (B) Western blot analysis showing that knockdown of SET8 in DNMT3A/3B DKO cells led to elevated levels of UHRF1 and DNMT1 proteins. (C) Quantitative HPLC analysis showing that knockdown of SET8 in DNMT3A/3B DKO cells resulted in elevated global levels of DNA methylation. **P< 0.01. (D) Western blot analysis showing successful knockdown of SET8 and enrichment of G2/M cells by nocodazole treatment. (E) Cell cycle analysis of the cells in (D) by FACS. (F) Strategy for analyzing DNA methylation in G2/M phase cells. (G) Quantitative analysis of the levels of DNA methylation in G2/M phase derived from I-methionine. (H) Working model showing that SET8 and LSD1 play an opposite role in regulating global DNA methylation and do so by controlling UHRF1 and DNMT1 protein stability through a methylation-mediated protein degradation pathway.