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      Totipotency in the mouse

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          Abstract

          In mammals, the unicellular zygote starts the process of embryogenesis and differentiates into all types of somatic cells, including both fetal and extraembryonic lineages—in a highly organized manner to eventually give rise to an entire multicellular organism comprising more than 200 different tissue types. This feature is referred to as totipotency. Upon fertilization, oocyte maternal factors epigenetically reprogram the genomes of the terminally differentiated oocyte and spermatozoon and turn the zygote into a totipotent cell. Today, we still do not fully understand the molecular properties of totipotency. In this review, we discuss recent findings on the molecular signature and mechanism of transcriptional regulation networks in the totipotent mouse embryo.

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          DNMT3L connects unmethylated lysine 4 of histone H3 to de novo methylation of DNA.

          Steen Ooi, Chen Qiu, Emily Bernstein … (2007)
          Mammals use DNA methylation for the heritable silencing of retrotransposons and imprinted genes and for the inactivation of the X chromosome in females. The establishment of patterns of DNA methylation during gametogenesis depends in part on DNMT3L, an enzymatically inactive regulatory factor that is related in sequence to the DNA methyltransferases DNMT3A and DNMT3B. The main proteins that interact in vivo with the product of an epitope-tagged allele of the endogenous Dnmt3L gene were identified by mass spectrometry as DNMT3A2, DNMT3B and the four core histones. Peptide interaction assays showed that DNMT3L specifically interacts with the extreme amino terminus of histone H3; this interaction was strongly inhibited by methylation at lysine 4 of histone H3 but was insensitive to modifications at other positions. Crystallographic studies of human DNMT3L showed that the protein has a carboxy-terminal methyltransferase-like domain and an N-terminal cysteine-rich domain. Cocrystallization of DNMT3L with the tail of histone H3 revealed that the tail bound to the cysteine-rich domain of DNMT3L, and substitution of key residues in the binding site eliminated the H3 tail-DNMT3L interaction. These data indicate that DNMT3L recognizes histone H3 tails that are unmethylated at lysine 4 and induces de novo DNA methylation by recruitment or activation of DNMT3A2.
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            Targeted mutation of the DNA methyltransferase gene results in embryonic lethality

            En Li, Timothy Bestor, Rudolf Jaenisch (1992)
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              Meiotic catastrophe and retrotransposon reactivation in male germ cells lacking Dnmt3L.

              Déborah Bourc'his, Timothy Bestor (2004)
              Mammalian genomes employ heritable cytosine methylation in the long-term silencing of retrotransposons and genes subject to genomic imprinting and X chromosome inactivation. Little is known of the mechanisms that direct cytosine methylation to specific sequences. Here we show that DNA methyltransferase 3-like (Dnmt3L (ref. 1)) is expressed in testes during a brief perinatal period in the non-dividing precursors of spermatogonial stem cells at a stage where retrotransposons undergo de novo methylation. Deletion of the Dnmt3L gene prevented the de novo methylation of both long-terminal-repeat (LTR) and non-LTR retrotransposons, which were transcribed at high levels in spermatogonia and spermatocytes. Loss of Dnmt3L from early germ cells also caused meiotic failure in spermatocytes, which do not express Dnmt3L. Whereas dispersed repeated sequences were demethylated in mutant germ cells, tandem repeats in pericentric regions were methylated normally. This result indicates that the Dnmt3L protein might have a function in the de novo methylation of dispersed repeated sequences in a premeiotic genome scanning process that occurs in male germ cells at about the time of birth.
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                Author and article information

                Contributors
                Hans R. Schöler: office@mpi-muenster.mpg.de
                Journal
                Journal ID (nlm-ta): J Mol Med (Berl)
                Journal ID (iso-abbrev): J. Mol. Med
                Title: Journal of Molecular Medicine (Berlin, Germany)
                Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )
                ISSN (Print): 0946-2716
                ISSN (Electronic): 1432-1440
                Publication date (Electronic): 19 January 2017
                Publication date PMC-release: 19 January 2017
                Publication date (Print): 2017
                Volume: 95
                Issue: 7
                Pages: 687-694
                Affiliations
                [1 ]ISNI 0000 0004 0491 9305, GRID grid.461801.a, Department of Cell and Developmental Biology, , Max Planck Institute for Molecular Biomedicine, ; Röntgenstrasse 20, 48149 Münster, Germany
                [2 ]ISNI 0000 0001 2204 9268, GRID grid.410736.7, Department of Histology and Embryology, , Harbin Medical University, ; 194 Xuefu Road, Nangang District, Harbin, 150081 China
                [3 ]ISNI 0000 0001 2172 9288, GRID grid.5949.1, Medical Faculty, , University of Münster, ; Domagkstr. 3, 48149 Münster, Germany
                Article
                Publisher ID: 1509
                DOI: 10.1007/s00109-017-1509-5
                PMC ID: 5487595
                PubMed ID: 28102431
                SO-VID: f724b0bf-93ed-4f88-8685-7ebe502f2177
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.

                History
                Date received : 31 October 2016
                Date revision received : 20 December 2016
                Date accepted : 12 January 2017
                Funding
                Funded by: Max-Planck-Gesellschaft (DE)
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: R01HD059946-01
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © Springer-Verlag GmbH Germany 2017

                ScienceOpen disciplines: Molecular medicine
                Keywords: totipotency,zygote,transcription factors
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: totipotency, zygote, transcription factors

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