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      Epigenetic integrity of paternal imprints enhances the developmental potential of androgenetic haploid embryonic stem cells

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          Abstract

          The use of two inhibitors of Mek1/2 and Gsk3β (2i) promotes the generation of mouse diploid and haploid embryonic stem cells (ESCs) from the inner cell mass of biparental and uniparental blastocysts, respectively. However, a system enabling long-term maintenance of imprints in ESCs has proven challenging. Here, we report that the use of a two-step a2i (alternative two inhibitors of Src and Gsk3β, TSa2i) derivation/culture protocol results in the establishment of androgenetic haploid ESCs (AG-haESCs) with stable DNA methylation at paternal DMRs (differentially DNA methylated regions) up to passage 60 that can efficiently support generating mice upon oocyte injection. We also show coexistence of H3K9me3 marks and ZFP57 bindings with intact DMR methylations. Furthermore, we demonstrate that TSa2i-treated AG-haESCs are a heterogeneous cell population regarding paternal DMR methylation. Strikingly, AG-haESCs with late passages display increased paternal-DMR methylations and improved developmental potential compared to early-passage cells, in part through the enhanced proliferation of H19-DMR hypermethylated cells. Together, we establish AG-haESCs that can long-term maintain paternal imprints.

          Supplementary Information

          The online version contains supplementary material available at 10.1007/s13238-021-00890-3.

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          Establishment in culture of pluripotential cells from mouse embryos.

          Sydney M. Evans, H Kaufman (1981)
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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.
            Article 0 comments Cited 450 times – based on 0 reviews     Review now
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              The ground state of embryonic stem cell self-renewal.

              Qi-Long Ying, Jason Wray, Jennifer Nichols … (2008)
              In the three decades since pluripotent mouse embryonic stem (ES) cells were first described they have been derived and maintained by using various empirical combinations of feeder cells, conditioned media, cytokines, growth factors, hormones, fetal calf serum, and serum extracts. Consequently ES-cell self-renewal is generally considered to be dependent on multifactorial stimulation of dedicated transcriptional circuitries, pre-eminent among which is the activation of STAT3 by cytokines (ref. 8). Here we show, however, that extrinsic stimuli are dispensable for the derivation, propagation and pluripotency of ES cells. Self-renewal is enabled by the elimination of differentiation-inducing signalling from mitogen-activated protein kinase. Additional inhibition of glycogen synthase kinase 3 consolidates biosynthetic capacity and suppresses residual differentiation. Complete bypass of cytokine signalling is confirmed by isolating ES cells genetically devoid of STAT3. These findings reveal that ES cells have an innate programme for self-replication that does not require extrinsic instruction. This property may account for their latent tumorigenicity. The delineation of minimal requirements for self-renewal now provides a defined platform for the precise description and dissection of the pluripotent state.
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                Author and article information

                Contributors
                Jinsong Li: jsli@sibcb.ac.cn
                Journal
                Journal ID (nlm-ta): Protein Cell
                Journal ID (iso-abbrev): Protein Cell
                Title: Protein & Cell
                Publisher: Higher Education Press (Beijing )
                ISSN (Print): 1674-800X
                ISSN (Electronic): 1674-8018
                Publication date (Electronic): 5 December 2021
                Publication date PMC-release: 5 December 2021
                Publication date (Print): February 2022
                Volume: 13
                Issue: 2
                Pages: 102-119
                Affiliations
                [1 ]GRID grid.410726.6, ISNI 0000 0004 1797 8419, State Key Laboratory of Cell Biology, Shanghai Key Laboratory of Molecular Andrology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, , University of Chinese Academy of Sciences, Chinese Academy of Sciences, ; Shanghai, 200031 China
                [2 ]GRID grid.440637.2, ISNI 0000 0004 4657 8879, School of Life Science and Technology, , ShanghaiTech University, ; Shanghai, 201210 China
                [3 ]GRID grid.410726.6, ISNI 0000 0004 1797 8419, Animal Core Facility, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, , Chinese Academy of Sciences, University of Chinese Academy of Sciences, ; Shanghai, 200031 China
                [4 ]GRID grid.410726.6, ISNI 0000 0004 1797 8419, School of Life Science, , Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, ; Hangzhou, 310024 China
                Article
                Publisher ID: 890
                DOI: 10.1007/s13238-021-00890-3
                PMC ID: 8783938
                PubMed ID: 34865203
                SO-VID: 93979796-6bf7-45f7-bba7-50a35bbdacb7
                Copyright © © The Author(s) 2022, corrected publication 2022
                License:

                Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 29 July 2021
                Date accepted : 26 September 2021
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2022

                Keywords: paternal imprints,androgenetic haploid escs,dmrs,semi-cloned mice,alternative 2i
                Data availability:
                Keywords: paternal imprints, androgenetic haploid escs, dmrs, semi-cloned mice, alternative 2i

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