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DNMT3B isoforms without catalytic activity stimulate gene body methylation as accessory proteins in somatic cells

Author

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  • Christopher E. Duymich

    (USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California)

  • Jessica Charlet

    (USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California)

  • Xiaojing Yang

    (USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California)

  • Peter A. Jones

    (USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California
    Present address: Van Andel Research Institute, Grand Rapids, Michigan 49503, USA.)

  • Gangning Liang

    (USC Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California)

Abstract

Promoter DNA methylation is a key epigenetic mechanism for stable gene silencing, but is correlated with expression when located in gene bodies. Maintenance and de novo DNA methylation by catalytically active DNA methyltransferases (DNMT1 and DNMT3A/B) require accessory proteins such as UHRF1 and DNMT3L. DNMT3B isoforms are widely expressed, although some do not have active catalytic domains and their expression can be altered during cell development and tumourigenesis, questioning their biological roles. Here, we show that DNMT3B isoforms stimulate gene body methylation and re-methylation after methylation-inhibitor treatment. This occurs independently of the isoforms’ catalytic activity, demonstrating a similar functional role to the accessory protein DNMT3L, which is only expressed in undifferentiated cells and recruits DNMT3A to initiate DNA methylation. This unexpected role for DNMT3B suggests that it might substitute for the absent accessory protein DNMT3L to recruit DNMT3A in somatic cells.

Suggested Citation

  • Christopher E. Duymich & Jessica Charlet & Xiaojing Yang & Peter A. Jones & Gangning Liang, 2016. "DNMT3B isoforms without catalytic activity stimulate gene body methylation as accessory proteins in somatic cells," Nature Communications, Nature, vol. 7(1), pages 1-9, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11453
    DOI: 10.1038/ncomms11453
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    1. Antonella Fazio & Dora Bordoni & Jan W. P. Kuiper & Saskia Weber-Stiehl & Stephanie T. Stengel & Philipp Arnold & David Ellinghaus & Go Ito & Florian Tran & Berith Messner & Anna Henning & Joana P. Be, 2022. "DNA methyltransferase 3A controls intestinal epithelial barrier function and regeneration in the colon," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    2. Feng Wang & Yang Xu & Robert Wang & Beatrice Zhang & Noah Smith & Amber Notaro & Samantha Gaerlan & Eric Kutschera & Kathryn E. Kadash-Edmondson & Yi Xing & Lan Lin, 2023. "TEQUILA-seq: a versatile and low-cost method for targeted long-read RNA sequencing," Nature Communications, Nature, vol. 14(1), pages 1-15, December.

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