Two distinct modes of DNMT1 recruitment ensure stable maintenance DNA methylation.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
06 03 2020
Historique:
received: 24 04 2019
accepted: 10 02 2020
entrez: 8 3 2020
pubmed: 8 3 2020
medline: 24 6 2020
Statut: epublish

Résumé

Stable inheritance of DNA methylation is critical for maintaining differentiated phenotypes in multicellular organisms. We have recently identified dual mono-ubiquitylation of histone H3 (H3Ub2) by UHRF1 as an essential mechanism to recruit DNMT1 to chromatin. Here, we show that PCNA-associated factor 15 (PAF15) undergoes UHRF1-dependent dual mono-ubiquitylation (PAF15Ub2) on chromatin in a DNA replication-coupled manner. This event will, in turn, recruit DNMT1. During early S-phase, UHRF1 preferentially ubiquitylates PAF15, whereas H3Ub2 predominates during late S-phase. H3Ub2 is enhanced under PAF15 compromised conditions, suggesting that H3Ub2 serves as a backup for PAF15Ub2. In mouse ES cells, loss of PAF15Ub2 results in DNA hypomethylation at early replicating domains. Together, our results suggest that there are two distinct mechanisms underlying replication timing-dependent recruitment of DNMT1 through PAF15Ub2 and H3Ub2, both of which are prerequisite for high fidelity DNA methylation inheritance.

Identifiants

pubmed: 32144273
doi: 10.1038/s41467-020-15006-4
pii: 10.1038/s41467-020-15006-4
pmc: PMC7060239
doi:

Substances chimiques

CCAAT-Enhancer-Binding Proteins 0
Chromatin 0
DNA (Cytosine-5-)-Methyltransferase 1 EC 2.1.1.37
UHRF1 protein, human EC 2.3.2.27
Ubiquitin-Protein Ligases EC 2.3.2.27

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1222

Références

Schübeler, D. Function and information content of DNA methylation. Nature 517, 321–326 (2015).
pubmed: 25592537 doi: 10.1038/nature14192
Jones, P. A. & Liang, G. Rethinking how DNA methylation patterns are maintained. Nat. Rev. Genet. 10, 805–811 (2009).
pubmed: 19789556 pmcid: 2848124 doi: 10.1038/nrg2651
Edwards, J. R., Yarychkivska, O., Boulard, M. & Bestor, T. H. DNA methylation and DNA methyltransferases. Epigenetics Chromatin 10, 23 (2017).
pubmed: 28503201 pmcid: 5422929 doi: 10.1186/s13072-017-0130-8
Leonhardt, H., Page, A. W., Weier, H. U. & Bestor, T. H. A targeting sequence directs DNA methyltransferase to sites of DNA replication in mammalian nuclei. Cell 71, 865–873 (1992).
pubmed: 1423634 doi: 10.1016/0092-8674(92)90561-P
Takeshita, K. et al. Structural insight into maintenance methylation by mouse DNA methyltransferase 1 (Dnmt1). PNAS 108, 9055–9059 (2011).
pubmed: 21518897 doi: 10.1073/pnas.1019629108
Syeda, F. et al. The replication focus targeting sequence (RFTS) domain is a DNA-competitive inhibitor of Dnmt1. J. Biol. Chem. 286, 15344–15351 (2011).
pubmed: 21389349 pmcid: 3083197 doi: 10.1074/jbc.M110.209882
Bostick, M. et al. UHRF1 plays a role in maintaining DNA methylation in mammalian cells. Science 317, 1760–1764 (2007).
pubmed: 17673620 doi: 10.1126/science.1147939
Sharif, J. et al. The SRA protein Np95 mediates epigenetic inheritance by recruiting Dnmt1 to methylated DNA. Nature 450, 908–912 (2007).
pubmed: 17994007 doi: 10.1038/nature06397
Arita, K., Ariyoshi, M., Tochio, H., Nakamura, Y. & Shirakawa, M. Recognition of hemi-methylated DNA by the SRA protein UHRF1 by a base-flipping mechanism. Nature 455, 818–821 (2008).
pubmed: 18772891 doi: 10.1038/nature07249
Hashimoto, H. et al. The SRA domain of UHRF1 flips 5-methylcytosine out of the DNA helix. Nature 455, 826–829 (2008).
pubmed: 18772888 pmcid: 2602803 doi: 10.1038/nature07280
Avvakumov, G. V. et al. Structural basis for recognition of hemi-methylated DNA by the SRA domain of human UHRF1. Nature 455, 822–825 (2008).
pubmed: 18772889 doi: 10.1038/nature07273
Rothbart, S. B. et al. Association of UHRF1 with methylated H3K9 directs the maintenance of DNA methylation. Nat. Struct. Mol. Biol. 19, 1155–1160 (2012).
pubmed: 23022729 pmcid: 3492551 doi: 10.1038/nsmb.2391
Rajakumara, E. et al. PHD finger recognition of unmodified histone H3R2 links UHRF1 to regulation of euchromatic gene expression. Mol. Cell 43, 275–284 (2011).
pubmed: 21777816 pmcid: 4691841 doi: 10.1016/j.molcel.2011.07.006
Arita, K. et al. Recognition of modification status on a histone H3 tail by linked histone reader modules of the epigenetic regulator UHRF1. PNAS 109, 12950–12955 (2012).
pubmed: 22837395 doi: 10.1073/pnas.1203701109
Ferry, L. et al. Methylation of DNA ligase 1 by G9a/GLP recruits UHRF1 to replicating DNA and regulates DNA methylation. Mol. Cell 67, 550–565.e5 (2017).
pubmed: 28803780 doi: 10.1016/j.molcel.2017.07.012
Kori, S. et al. Structure of the UHRF1 tandem Tudor domain bound to a methylated non-histone protein, LIG1, reveals rules for binding and regulation. Structure 27, 485–496.e7 (2018).
doi: 10.1016/j.str.2018.11.012
Nishiyama, A. et al. Uhrf1-dependent H3K23 ubiquitylation couples maintenance DNA methylation and replication. Nature 502, 249–253 (2013).
pubmed: 24013172 doi: 10.1038/nature12488
Qin, W. et al. DNA methylation requires a DNMT1 ubiquitin interacting motif (UIM) and histone ubiquitination. Cell Res. 25, 911–929 (2015).
pubmed: 26065575 pmcid: 4528052 doi: 10.1038/cr.2015.72
Harrison, J. S. et al. Hemi-methylated DNA regulates DNA methylation inheritance through allosteric activation of H3 ubiquitylation by UHRF1. Elife 5, 818 (2016).
doi: 10.7554/eLife.17101
Vaughan, R. M. et al. Chromatin structure and its chemical modifications regulate the ubiquitin ligase substrate selectivity of UHRF1. PNAS 115, 8775–8780 (2018).
pubmed: 30104358 doi: 10.1073/pnas.1806373115
DaRosa, P. A. et al. A bifunctional role for the UHRF1 UBL domain in the control of hemi-methylated DNA-dependent histone ubiquitylation. Mol. Cell 72, 753–765.e6 (2018).
pubmed: 30392931 pmcid: 6239910 doi: 10.1016/j.molcel.2018.09.029
Foster, B. M. et al. Critical role of the UBL domain in stimulating the E3 ubiquitin ligase activity of UHRF1 toward chromatin. Mol. Cell 72, 739–752.e9 (2018).
pubmed: 30392929 pmcid: 6242706 doi: 10.1016/j.molcel.2018.09.028
Ishiyama, S. et al. Structure of the Dnmt1 reader module complexed with a unique two-mono-ubiquitin mark on histone H3 reveals the basis for DNA methylation maintenance. Mol. Cell 68, 350–360.e7 (2017).
pubmed: 29053958 doi: 10.1016/j.molcel.2017.09.037
Li, T. et al. Structural and mechanistic insights into UHRF1-mediated DNMT1 activation in the maintenance DNA methylation. Nucleic Acids Res. 14, 204–3231 (2018).
Yamaguchi, L. et al. Usp7-dependent histone H3 deubiquitylation regulates maintenance of DNA methylation. Sci. Rep. 7, 55 (2017).
pubmed: 28246399 pmcid: 5427934 doi: 10.1038/s41598-017-00136-5
Cheng, J. et al. Molecular mechanism for USP7-mediated DNMT1 stabilization by acetylation. Nat. Commun. 6, 7023 (2015).
pubmed: 25960197 pmcid: 4432644 doi: 10.1038/ncomms8023
Felle, M. et al. The USP7/Dnmt1 complex stimulates the DNA methylation activity of Dnmt1 and regulates the stability of UHRF1. Nucleic Acids Res. 39, 8355–8365 (2011).
pubmed: 21745816 pmcid: 3201865 doi: 10.1093/nar/gkr528
Du, Z. et al. DNMT1 stability is regulated by proteins coordinating deubiquitination and acetylation-driven ubiquitination. Sci. Signal. 3, ra80–ra80 (2010).
pubmed: 21045206 pmcid: 3116231 doi: 10.1126/scisignal.2001462
Easwaran, H. P., Schermelleh, L., Leonhardt, H. & Cardoso, M. C. Replication‐independent chromatin loading of Dnmt1 during G2 and M phases. EMBO Rep. 5, 1181–1186 (2004).
pubmed: 15550930 pmcid: 1299190 doi: 10.1038/sj.embor.7400295
Borodovsky, A. et al. A novel active site-directed probe specific for deubiquitylating enzymes reveals proteasome association of USP14. EMBO J. 20, 5187–5196 (2001).
pubmed: 11566882 pmcid: 125629 doi: 10.1093/emboj/20.18.5187
Dimova, N. V. et al. APC/C-mediated multiple monoubiquitylation provides an alternative degradation signal for cyclin B1. Nat. Cell Biol. 14, 168–176 (2012).
pubmed: 22286100 pmcid: 3278798 doi: 10.1038/ncb2425
Emanuele, M. J., Ciccia, A., Elia, A. E. H. & Elledge, S. J. Proliferating cell nuclear antigen (PCNA)-associated KIAA0101/PAF15 protein is a cell cycle-regulated anaphase-promoting complex/cyclosome substrate. PNAS 108, 9845–9850 (2011).
pubmed: 21628590 doi: 10.1073/pnas.1106136108
Povlsen, L. K. et al. Systems-wide analysis of ubiquitylation dynamics reveals a key role for PAF15 ubiquitylation in DNA-damage bypass. Nat. Cell Biol. 14, 1089–1098 (2012).
pubmed: 23000965 doi: 10.1038/ncb2579
Blow, J. J. & Laskey, R. A. Initiation of DNA replication in nuclei and purified DNA by a cell-free extract of Xenopus eggs. Cell 47, 577–587 (1986).
pubmed: 3779837 doi: 10.1016/0092-8674(86)90622-7
Misaki, T. et al. The replication foci targeting sequence (RFTS) of DNMT1 functions as a potent histone H3 binding domain regulated by autoinhibition. Biochem. Biophys. Res. Commun. 470, 741–747 (2016).
pubmed: 26774338 doi: 10.1016/j.bbrc.2016.01.029
Karg, E. et al. Ubiquitome analysis reveals PCNA-associated factor 15 (PAF15) as a specific ubiquitination target of UHRF1 in embryonic stem cells. J. Mol. Biol. 429, 3814–3824 (2017).
pubmed: 29055779 doi: 10.1016/j.jmb.2017.10.014
Herce, H. D., Deng, W., Helma, J., Leonhardt, H. & Cardoso, M. C. Visualization and targeted disruption of protein interactions in living cells. Nat. Commun. 4, 2660 (2013).
pubmed: 24154492 pmcid: 3826628 doi: 10.1038/ncomms3660
Kurimoto, K. et al. Quantitative dynamics of chromatin remodeling during germ cell specification from mouse embryonic stem cells. Cell Stem Cell 16, 517–532 (2015).
pubmed: 25800778 doi: 10.1016/j.stem.2015.03.002
Marks, H. et al. The transcriptional and epigenomic foundations of ground state pluripotency. Cell 149, 590–604 (2012).
pubmed: 22541430 pmcid: 3398752 doi: 10.1016/j.cell.2012.03.026
Karmodiya, K., Krebs, A. R., Oulad-Abdelghani, M., Kimura, H. & Tora, L. H3K9 and H3K14 acetylation co-occur at many gene regulatory elements, while H3K14ac marks a subset of inactive inducible promoters in mouse embryonic stem cells. BMC Genomics 13, 424 (2012).
pubmed: 22920947 pmcid: 3473242 doi: 10.1186/1471-2164-13-424
Timp, W. et al. Large hypomethylated blocks as a universal defining epigenetic alteration in human solid tumors. Genome Med. 6, 61–11 (2014).
pubmed: 25191524 pmcid: 4154522 doi: 10.1186/s13073-014-0061-y
Zhou, W. et al. DNA methylation loss in late-replicating domains is linked to mitotic cell division. Nat. Genet. 50, 591–602 (2018).
pubmed: 29610480 pmcid: 5893360 doi: 10.1038/s41588-018-0073-4
Hiratani, I. et al. Genome-wide dynamics of replication timing revealed by in vitro models of mouse embryogenesis. Genome Res. 20, 155–169 (2010).
pubmed: 19952138 pmcid: 2813472 doi: 10.1101/gr.099796.109
Aran, D., Toperoff, G., Rosenberg, M. & Hellman, A. Replication timing-related and gene body-specific methylation of active human genes. Hum. Mol. Genet. 20, 670–680 (2011).
pubmed: 21112978 doi: 10.1093/hmg/ddq513 pmcid: 21112978
Branzei, D. & Foiani, M. Maintaining genome stability at the replication fork. Nat. Rev. Mol. Cell Biol. 11, 208–219 (2010).
pubmed: 20177396 doi: 10.1038/nrm2852
Li, E., Bestor, T. H. & Jaenisch, R. Targeted mutation of the DNA methyltransferase gene results in embryonic lethality. Cell 69, 915–926 (1992).
pubmed: 1606615 doi: 10.1016/0092-8674(92)90611-F pmcid: 1606615
Amrani, Y. M. et al. The Paf oncogene is essential for hematopoietic stem cell function and development. J. Exp. Med. 208, 1757–1765 (2011).
pubmed: 21844206 pmcid: 3171089 doi: 10.1084/jem.20102170
De March, M. et al. p15PAF binding to PCNA modulates the DNA sliding surface. Nucleic Acids Res. 79, 1233–9828 (2018).
Gonzalez-Magaña, A. et al. Double monoubiquitination modifies the molecular recognition properties of p15PAF promoting binding to the reader module of Dnmt1. ACS Chem. Biol. 14, 2315–2326 (2019).
pubmed: 31479228
Tsuchiya, H. et al. In vivo ubiquitin linkage-type analysis reveals that the Cdc48-Rad23/Dsk2 axis contributes to K48-linked chain specificity of the proteasome. Mol. Cell 66, 488.e7–502.e7 (2017).
doi: 10.1016/j.molcel.2017.04.024
Deutsch, E. W. et al. The ProteomeXchange consortium in 2017: supporting the cultural change in proteomics public data deposition. Nucleic Acids Res. 45, D1100–D1106 (2017).
pubmed: 27924013 doi: 10.1093/nar/gkw936
Perez-Riverol, Y. et al. The PRIDE database and related tools and resources in 2019: improving support for quantification data. Nucleic Acids Res. 47, D442–D450 (2019).
pubmed: 30395289 doi: 10.1093/nar/gky1106
Kabsch, W. XDS. Acta Crystallogr. D Biol. Crystallogr. 66, 125–132 (2010).
pubmed: 20124692 pmcid: 2815665 doi: 10.1107/S0907444909047337
Evans, P. R. & Murshudov, G. N. How good are my data and what is the resolution? Acta Crystallogr. D Biol. Crystallogr. 69, 1204–1214 (2013).
pubmed: 23793146 pmcid: 3689523 doi: 10.1107/S0907444913000061
McCoy, A. J. et al. Phaser crystallographic software. J. Appl. Crystallogr. 40, 658–674 (2007).
pubmed: 19461840 pmcid: 2483472 doi: 10.1107/S0021889807021206
Afonine, P. V. et al. Towards automated crystallographic structure refinement with phenix.refine. Acta Crystallogr. D Biol. Crystallogr. 68, 352–367 (2012).
pubmed: 22505256 pmcid: 3322595 doi: 10.1107/S0907444912001308
Goda, N. et al. An optimized Npro-based method for the expression and purification of intrinsically disordered proteins for an NMR study. Intrinsically Disord. Proteins 3, e1011004 (2015).
pubmed: 28232886 pmcid: 5314886 doi: 10.1080/21690707.2015.1011004
Shimizu, N. et al. Software development for analysis of small-angle x-ray scattering data. AIP Conf. Proc. 1741, 050017 (2016).
Orthaber, D., Bergmann, A. & Glatter, O. SAXS experiments on absolute scale with Kratky systems using water as a secondary standard. J. Appl. Crystallogr. 33, 218–225 (2000).
doi: 10.1107/S0021889899015216
Yonezawa, K., Takahashi, M., Yatabe, K., Nagatani, Y. & Shimizu, N. Software for serial data analysis measured by SEC-SAXS/UV-Vis spectroscopy. AIP Conf. Proc. 2054, 060082 (2019).
Svergun, D. I. Determination of the regularization parameter in indirect-transform methods using perceptual criteria. J. Appl. Crystallogr. 25, 495–503 (1992).
doi: 10.1107/S0021889892001663
Mulholland, C. B. et al. A modular open platform for systematic functional studies under physiological conditions. Nucleic Acids Res. 43, e112–e112 (2015).
pubmed: 26007658 pmcid: 4787826 doi: 10.1093/nar/gkv550
Tsukamoto, T. et al. Visualization of gene activity in living cells. Nat. Cell Biol. 2, 871–878 (2000).
pubmed: 11146650 doi: 10.1038/35046510
Ran, F. A. et al. Genome engineering using the CRISPR-Cas9 system. Nat. Protoc. 8, 2281–2308 (2013).
pubmed: 3969860 pmcid: 3969860 doi: 10.1038/nprot.2013.143
Gutschner, T., Haemmerle, M., Genovese, G., Draetta, G. F. & Chin, L. Post-translational regulation of Cas9 during G1 enhances homology-directed repair. Cell Rep. 14, 1555–1566 (2016).
pubmed: 26854237 doi: 10.1016/j.celrep.2016.01.019
Boyle, P. et al. Gel-free multiplexed reduced representation bisulfite sequencing for large-scale DNA methylation profiling. Genome Biol. 13, R92 (2012).
pubmed: 23034176 pmcid: 3491420 doi: 10.1186/gb-2012-13-10-r92
Akalin, A. et al. methylKit: a comprehensive R package for the analysis of genome-wide DNA methylation profiles. Genome Biol. 13, R87 (2012).
pubmed: 23034086 pmcid: 3491415 doi: 10.1186/gb-2012-13-10-r87
Illingworth, R. S. et al. Orphan CpG islands identify numerous conserved promoters in the mammalian genome. PLoS Genet. 6, e1001134 (2010).
pubmed: 20885785 pmcid: 2944787 doi: 10.1371/journal.pgen.1001134
Zhang, Y. et al. Model-based analysis of ChIP-Seq (MACS). Genome Biol. 9, R137–R139 (2008).
pubmed: 18798982 pmcid: 2592715 doi: 10.1186/gb-2008-9-9-r137
Meilinger, D. et al. Np95 interacts with de novo DNA methyltransferases, Dnmt3a and Dnmt3b, and mediates epigenetic silencing of the viral CMV promoter in embryonic stem cells. EMBO Rep. 10, 1259–1264 (2009).
pubmed: 19798101 pmcid: 2756565 doi: 10.1038/embor.2009.201

Auteurs

Atsuya Nishiyama (A)

Division of Cancer Cell Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan. anishiya@ims.u-tokyo.ac.jp.

Christopher B Mulholland (CB)

Department of Biology II and Center for Integrated Protein Science Munich (CIPSM), Human Biology and BioImaging, Ludwig-Maximilians-Universität München, 82152, Planegg-Martinsried, Germany.

Sebastian Bultmann (S)

Department of Biology II and Center for Integrated Protein Science Munich (CIPSM), Human Biology and BioImaging, Ludwig-Maximilians-Universität München, 82152, Planegg-Martinsried, Germany.

Satomi Kori (S)

Structure Biology Laboratory, Graduate School of Medical Life Science, Yokohama City University, 1-7-29, Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa, Japan.

Akinori Endo (A)

Laboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.

Yasushi Saeki (Y)

Laboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.

Weihua Qin (W)

Department of Biology II and Center for Integrated Protein Science Munich (CIPSM), Human Biology and BioImaging, Ludwig-Maximilians-Universität München, 82152, Planegg-Martinsried, Germany.

Carina Trummer (C)

Department of Biology II and Center for Integrated Protein Science Munich (CIPSM), Human Biology and BioImaging, Ludwig-Maximilians-Universität München, 82152, Planegg-Martinsried, Germany.

Yoshie Chiba (Y)

Division of Cancer Cell Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan.

Haruka Yokoyama (H)

Structure Biology Laboratory, Graduate School of Medical Life Science, Yokohama City University, 1-7-29, Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa, Japan.

Soichiro Kumamoto (S)

Division of Cancer Cell Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan.

Toru Kawakami (T)

Laboratory of Protein Organic Chemistry, Institute for Protein Research, Osaka University, Suita, Osaka, Japan.

Hironobu Hojo (H)

Laboratory of Protein Organic Chemistry, Institute for Protein Research, Osaka University, Suita, Osaka, Japan.

Genta Nagae (G)

The Research Center for Advanced Science and Technology, University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo, Japan.

Hiroyuki Aburatani (H)

The Research Center for Advanced Science and Technology, University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo, Japan.

Keiji Tanaka (K)

Laboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.

Kyohei Arita (K)

Structure Biology Laboratory, Graduate School of Medical Life Science, Yokohama City University, 1-7-29, Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa, Japan. aritak@yokohama-cu.ac.jp.

Heinrich Leonhardt (H)

Department of Biology II and Center for Integrated Protein Science Munich (CIPSM), Human Biology and BioImaging, Ludwig-Maximilians-Universität München, 82152, Planegg-Martinsried, Germany. h.leonhardt@lmu.de.

Makoto Nakanishi (M)

Division of Cancer Cell Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, Japan. mkt-naka@ims.u-tokyo.ac.jp.

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