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  • 1
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    Epigenetic reprogramming in mammalian development (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-11
    Description: DNA methylation is a major epigenetic modification of the genome that regulates crucial aspects of its function. Genomic methylation patterns in somatic differentiated cells are generally stable and heritable. However, in mammals there are at least two developmental periods-in germ cells and in preimplantation embryos-in which methylation patterns are reprogrammed genome wide, generating cells with a broad developmental potential. Epigenetic reprogramming in germ cells is critical for imprinting; reprogramming in early embryos also affects imprinting. Reprogramming is likely to have a crucial role in establishing nuclear totipotency in normal development and in cloned animals, and in the erasure of acquired epigenetic information. A role of reprogramming in stem cell differentiation is also envisaged. DNA methylation is one of the best-studied epigenetic modifications of DNA in all unicellular and multicellular organisms. In mammals and other vertebrates, methylation occurs predominantly at the symmetrical dinucleotide CpG (1-4). Symmetrical methylation and the discovery of a DNA methyltransferase that prefers a hemimethylated substrate, Dnmt1 (4), suggested a mechanism by which specific patterns of methylation in the genome could be maintained. Patterns imposed on the genome at defined developmental time points in precursor cells could be maintained by Dnmt1, and would lead to predetermined programs of gene expression during development in descendants of the precursor cells (5, 6). This provided a means to explain how patterns of differentiation could be maintained by populations of cells. In addition, specific demethylation events in differentiated tissues could then lead to further changes in gene expression as needed. Neat and convincing as this model is, it is still largely unsubstantiated. While effects of methylation on expression of specific genes, particularly imprinted ones (7) and some retrotransposons (8), have been demonstrated in vivo, it is still unclear whether or not methylation is involved in the control of gene expression during normal development (9-13). Although enzymes have been identified that can methylate DNA de novo (Dnmt3a and Dnmt3b) (14), it is unknown how specific patterns of methylation are established in the genome. Mechanisms for active demethylation have been suggested, but no enzymes have been identified that carry out this function in vivo (15-17). Genomewide alterations in methylation-brought about, for example, by knockouts of the methylase genes-result in embryo lethality or developmental defects, but the basis for abnormal development still remains to be discovered (7, 14). What is clear, however, is that in mammals there are developmental periods of genomewide reprogramming of methylation patterns in vivo. Typically, a substantial part of the genome is demethylated, and after some time remethylated, in a cell- or tissue-specific pattern. The developmental dynamics of these reprogramming events, as well as some of the enzymatic mechanisms involved and the biological purposes, are beginning to be understood. Here we look at what is known about reprogramming in mammals and discuss how it might relate to developmental potency and imprinting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reik, W -- Dean, W -- Walter, J -- New York, N.Y. -- Science. 2001 Aug 10;293(5532):1089-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Genetics and Imprinting, The Babraham Institute, Cambridge CB2 4AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11498579" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism ; Cell Differentiation ; Cloning, Organism ; *DNA Methylation ; Dosage Compensation, Genetic ; Embryo, Mammalian/*metabolism ; *Embryo, Nonmammalian ; *Embryonic and Fetal Development ; Female ; *Gene Expression Regulation, Developmental ; Genomic Imprinting ; Germ Cells/*metabolism ; Male ; Stem Cells/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Genome-wide erasure of DNA methylation in mouse primordial germ cells is affected by AID deficiency (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-01-26
    Description: Epigenetic reprogramming including demethylation of DNA occurs in mammalian primordial germ cells (PGCs) and in early embryos, and is important for the erasure of imprints and epimutations, and the return to pluripotency. The extent of this reprogramming and its molecular mechanisms are poorly understood. We previously showed that the cytidine deaminases AID and APOBEC1 can deaminate 5-methylcytosine in vitro and in Escherichia coli, and in the mouse are expressed in tissues in which demethylation occurs. Here we profiled DNA methylation throughout the genome by unbiased bisulphite next generation sequencing in wild-type and AID-deficient mouse PGCs at embryonic day (E)13.5. Wild-type PGCs revealed marked genome-wide erasure of methylation to a level below that of methylation deficient (Np95(-/-), also called Uhrf1(-/-)) embryonic stem cells, with female PGCs being less methylated than male ones. By contrast, AID-deficient PGCs were up to three times more methylated than wild-type ones; this substantial difference occurred throughout the genome, with introns, intergenic regions and transposons being relatively more methylated than exons. Relative hypermethylation in AID-deficient PGCs was confirmed by analysis of individual loci in the genome. Our results reveal that erasure of DNA methylation in the germ line is a global process, hence limiting the potential for transgenerational epigenetic inheritance. AID deficiency interferes with genome-wide erasure of DNA methylation patterns, indicating that AID has a critical function in epigenetic reprogramming and potentially in restricting the inheritance of epimutations in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2965733/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2965733/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Popp, Christian -- Dean, Wendy -- Feng, Suhua -- Cokus, Shawn J -- Andrews, Simon -- Pellegrini, Matteo -- Jacobsen, Steven E -- Reik, Wolf -- G0700098/Medical Research Council/United Kingdom -- R37 GM060398/GM/NIGMS NIH HHS/ -- R37 GM060398-11/GM/NIGMS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- England -- Nature. 2010 Feb 25;463(7284):1101-5. doi: 10.1038/nature08829.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Genetics and Imprinting, The Babraham Institute, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20098412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytidine Deaminase/*deficiency/genetics/*metabolism ; *DNA Methylation ; DNA Transposable Elements/genetics ; Embryo, Mammalian/cytology/embryology/metabolism ; Epigenesis, Genetic/genetics ; Exons/genetics ; Female ; *Genome/genetics ; Germ Cells/enzymology/*metabolism ; Introns/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/deficiency/genetics ; Octamer Transcription Factor-3/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Quantitative sequencing of 5-methylcytosine and 5-hydroxymethylcytosine at single-base resolution (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-28
    Description: 5-Methylcytosine can be converted to 5-hydroxymethylcytosine (5hmC) in mammalian DNA by the ten-eleven translocation (TET) enzymes. We introduce oxidative bisulfite sequencing (oxBS-Seq), the first method for quantitative mapping of 5hmC in genomic DNA at single-nucleotide resolution. Selective chemical oxidation of 5hmC to 5-formylcytosine (5fC) enables bisulfite conversion of 5fC to uracil. We demonstrate the utility of oxBS-Seq to map and quantify 5hmC at CpG islands (CGIs) in mouse embryonic stem (ES) cells and identify 800 5hmC-containing CGIs that have on average 3.3% hydroxymethylation. High levels of 5hmC were found in CGIs associated with transcriptional regulators and in long interspersed nuclear elements, suggesting that these regions might undergo epigenetic reprogramming in ES cells. Our results open new questions on 5hmC dynamics and sequence-specific targeting by TETs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Booth, Michael J -- Branco, Miguel R -- Ficz, Gabriella -- Oxley, David -- Krueger, Felix -- Reik, Wolf -- Balasubramanian, Shankar -- 095645/Wellcome Trust/United Kingdom -- 11961/Cancer Research UK/United Kingdom -- G0801156/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):934-7. doi: 10.1126/science.1220671. Epub 2012 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Cambridge, Cambridge CB2 1EW, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539555" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*analysis ; Animals ; *CpG Islands ; Cytosine/*analogs & derivatives/analysis/chemistry ; DNA/*chemistry/genetics ; DNA Methylation ; *Embryonic Stem Cells/physiology ; Epigenesis, Genetic ; Genes, Intracisternal A-Particle ; High-Throughput Nucleotide Sequencing ; Long Interspersed Nucleotide Elements ; Mice ; Oxidation-Reduction ; Rhenium/chemistry ; *Sequence Analysis, DNA ; Sulfites ; Transcription, Genetic ; Uracil/chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Dynamic regulation of 5-hydroxymethylcytosine in mouse ES cells and during differentiation (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-04-05
    Description: Methylation at the 5' position of cytosine in DNA has important roles in genome function and is dynamically reprogrammed during early embryonic and germ cell development. The mammalian genome also contains 5-hydroxymethylcytosine (5hmC), which seems to be generated by oxidation of 5-methylcytosine (5mC) by the TET family of enzymes that are highly expressed in embryonic stem (ES) cells. Here we use antibodies against 5hmC and 5mC together with high throughput sequencing to determine genome-wide patterns of methylation and hydroxymethylation in mouse wild-type and mutant ES cells and differentiating embryoid bodies. We find that 5hmC is mostly associated with euchromatin and that whereas 5mC is under-represented at gene promoters and CpG islands, 5hmC is enriched and is associated with increased transcriptional levels. Most, if not all, 5hmC in the genome depends on pre-existing 5mC and the balance between these two modifications is different between genomic regions. Knockdown of Tet1 and Tet2 causes downregulation of a group of genes that includes pluripotency-related genes (including Esrrb, Prdm14, Dppa3, Klf2, Tcl1 and Zfp42) and a concomitant increase in methylation of their promoters, together with an increased propensity of ES cells for extraembryonic lineage differentiation. Declining levels of TETs during differentiation are associated with decreased hydroxymethylation levels at the promoters of ES cell-specific genes together with increased methylation and gene silencing. We propose that the balance between hydroxymethylation and methylation in the genome is inextricably linked with the balance between pluripotency and lineage commitment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ficz, Gabriella -- Branco, Miguel R -- Seisenberger, Stefanie -- Santos, Fatima -- Krueger, Felix -- Hore, Timothy A -- Marques, C Joana -- Andrews, Simon -- Reik, Wolf -- G0801156/Medical Research Council/United Kingdom -- G0801727/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2011 May 19;473(7347):398-402. doi: 10.1038/nature10008. Epub 2011 Apr 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Genetics and Imprinting, The Babraham Institute, Cambridge CB22 3AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21460836" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Cell Differentiation/*genetics ; Cell Line ; Cell Lineage/genetics ; CpG Islands/genetics ; Cytosine/*analogs & derivatives/analysis/immunology/metabolism ; *DNA Methylation ; DNA-Binding Proteins/deficiency ; Down-Regulation ; Embryoid Bodies/cytology/metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Euchromatin/genetics/metabolism ; Exons/genetics ; *Gene Expression Regulation, Developmental ; Gene Silencing ; Genome/genetics ; Mice ; Pluripotent Stem Cells/cytology/metabolism ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins/deficiency ; Reproducibility of Results ; Sequence Analysis, DNA ; Transcription, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Epigenetics: Cellular memory erased in human embryos (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-08-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reik, Wolf -- Kelsey, Gavin -- 095645/Wellcome Trust/United Kingdom -- MR/K011332/1/Medical Research Council/United Kingdom -- England -- Nature. 2014 Jul 31;511(7511):540-1. doi: 10.1038/nature13648. Epub 2014 Jul 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Epigenetics Programme, Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK, and at the Centre for Trophoblast Research, University of Cambridge. [2] Wellcome Trust Sanger Institute, Cambridge. ; Epigenetics Programme, Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK, and at the Centre for Trophoblast Research, University of Cambridge.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Methylation ; DNA Transposable Elements/physiology ; Embryo, Mammalian/metabolism ; *Epigenomics ; Genomic Imprinting ; Humans
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    NANOG-dependent function of TET1 and TET2 in establishment of pluripotency (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-02-12
    Description: Molecular control of the pluripotent state is thought to reside in a core circuitry of master transcription factors including the homeodomain-containing protein NANOG, which has an essential role in establishing ground state pluripotency during somatic cell reprogramming. Whereas the genomic occupancy of NANOG has been extensively investigated, comparatively little is known about NANOG-associated proteins and their contribution to the NANOG-mediated reprogramming process. Using enhanced purification techniques and a stringent computational algorithm, we identify 27 high-confidence protein interaction partners of NANOG in mouse embryonic stem cells. These consist of 19 previously unknown partners of NANOG that have not been reported before, including the ten-eleven translocation (TET) family methylcytosine hydroxylase TET1. We confirm physical association of NANOG with TET1, and demonstrate that TET1, in synergy with NANOG, enhances the efficiency of reprogramming. We also find physical association and reprogramming synergy of TET2 with NANOG, and demonstrate that knockdown of TET2 abolishes the reprogramming synergy of NANOG with a catalytically deficient mutant of TET1. These results indicate that the physical interaction between NANOG and TET1/TET2 proteins facilitates reprogramming in a manner that is dependent on the catalytic activity of TET1/TET2. TET1 and NANOG co-occupy genomic loci of genes associated with both maintenance of pluripotency and lineage commitment in embryonic stem cells, and TET1 binding is reduced upon NANOG depletion. Co-expression of NANOG and TET1 increases 5-hydroxymethylcytosine levels at the top-ranked common target loci Esrrb and Oct4 (also called Pou5f1), resulting in priming of their expression before reprogramming to naive pluripotency. We propose that TET1 is recruited by NANOG to enhance the expression of a subset of key reprogramming target genes. These results provide an insight into the reprogramming mechanism of NANOG and uncover a new role for 5-methylcytosine hydroxylases in the establishment of naive pluripotency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3606645/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3606645/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Costa, Yael -- Ding, Junjun -- Theunissen, Thorold W -- Faiola, Francesco -- Hore, Timothy A -- Shliaha, Pavel V -- Fidalgo, Miguel -- Saunders, Arven -- Lawrence, Moyra -- Dietmann, Sabine -- Das, Satyabrata -- Levasseur, Dana N -- Li, Zhe -- Xu, Mingjiang -- Reik, Wolf -- Silva, Jose C R -- Wang, Jianlong -- 079249/Wellcome Trust/United Kingdom -- 086692/Wellcome Trust/United Kingdom -- 095645/Wellcome Trust/United Kingdom -- 1R01-GM095942-01A1/GM/NIGMS NIH HHS/ -- BB/H008071/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0700098/Medical Research Council/United Kingdom -- R01 GM095942/GM/NIGMS NIH HHS/ -- R01 HL112294/HL/NHLBI NIH HHS/ -- WT079249/Wellcome Trust/United Kingdom -- WT086692MA/Wellcome Trust/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2013 Mar 21;495(7441):370-4. doi: 10.1038/nature11925. Epub 2013 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23395962" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cellular Reprogramming/*physiology ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells ; Gene Expression Regulation, Developmental ; Genome ; Homeodomain Proteins/genetics/*metabolism ; Mice ; Protein Binding ; Proto-Oncogene Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Epigenetic reprogramming in plant and animal development (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-30
    Description: Epigenetic modifications of the genome are generally stable in somatic cells of multicellular organisms. In germ cells and early embryos, however, epigenetic reprogramming occurs on a genome-wide scale, which includes demethylation of DNA and remodeling of histones and their modifications. The mechanisms of genome-wide erasure of DNA methylation, which involve modifications to 5-methylcytosine and DNA repair, are being unraveled. Epigenetic reprogramming has important roles in imprinting, the natural as well as experimental acquisition of totipotency and pluripotency, control of transposons, and epigenetic inheritance across generations. Small RNAs and the inheritance of histone marks may also contribute to epigenetic inheritance and reprogramming. Reprogramming occurs in flowering plants and in mammals, and the similarities and differences illuminate developmental and reproductive strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989926/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989926/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Suhua -- Jacobsen, Steven E -- Reik, Wolf -- G0700098/Medical Research Council/United Kingdom -- GM60398/GM/NIGMS NIH HHS/ -- R37 GM060398/GM/NIGMS NIH HHS/ -- R37 GM060398-10/GM/NIGMS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Oct 29;330(6004):622-7. doi: 10.1126/science.1190614.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21030646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arabidopsis/embryology/*genetics ; Cellular Reprogramming ; *DNA Methylation ; DNA Transposable Elements ; Embryo, Mammalian/metabolism/physiology ; Embryo, Nonmammalian/metabolism/physiology ; Embryonic Development ; *Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental ; Gene Silencing ; Genomic Imprinting ; Germ Cells/growth & development/metabolism ; Histones/*metabolism ; Male ; Mammals/embryology/*genetics ; Protein Processing, Post-Translational
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    In utero effects. In utero undernourishment perturbs the adult sperm methylome and intergenerational metabolism (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-07-12
    Description: Adverse prenatal environments can promote metabolic disease in offspring and subsequent generations. Animal models and epidemiological data implicate epigenetic inheritance, but the mechanisms remain unknown. In an intergenerational developmental programming model affecting F2 mouse metabolism, we demonstrate that the in utero nutritional environment of F1 embryos alters the germline DNA methylome of F1 adult males in a locus-specific manner. Differentially methylated regions are hypomethylated and enriched in nucleosome-retaining regions. A substantial fraction is resistant to early embryo methylation reprogramming, which may have an impact on F2 development. Differential methylation is not maintained in F2 tissues, yet locus-specific expression is perturbed. Thus, in utero nutritional exposures during critical windows of germ cell development can impact the male germline methylome, associated with metabolic disease in offspring.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404520/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404520/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Radford, Elizabeth J -- Ito, Mitsuteru -- Shi, Hui -- Corish, Jennifer A -- Yamazawa, Kazuki -- Isganaitis, Elvira -- Seisenberger, Stefanie -- Hore, Timothy A -- Reik, Wolf -- Erkek, Serap -- Peters, Antoine H F M -- Patti, Mary-Elizabeth -- Ferguson-Smith, Anne C -- 095606/Wellcome Trust/United Kingdom -- 095645/Wellcome Trust/United Kingdom -- P30 DK036836/DK/NIDDK NIH HHS/ -- P30DK036836/DK/NIDDK NIH HHS/ -- R00 HD064793/HD/NICHD NIH HHS/ -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):1255903. doi: 10.1126/science.1255903. Epub 2014 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK. ; Research Division, Joslin Diabetes Center and Harvard Medical School, 1 Joslin Place, Boston, MA 02215, USA. ; The Babraham Institute, Babraham, Cambridge, and Wellcome Trust Sanger Institute, Hinxton, Cambridge, UK. ; Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland. Faculty of Sciences, University of Basel, Basel, Switzerland. Swiss Institute of Bioinformatics, Basel, Switzerland. ; Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland. Faculty of Sciences, University of Basel, Basel, Switzerland. ; Research Division, Joslin Diabetes Center and Harvard Medical School, 1 Joslin Place, Boston, MA 02215, USA. afsmith@mole.bio.cam.ac.uk mary.elizabeth.patti@joslin.harvard.edu. ; Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK. afsmith@mole.bio.cam.ac.uk mary.elizabeth.patti@joslin.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25011554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caloric Restriction ; *DNA Methylation ; Epigenesis, Genetic ; Female ; Fetal Nutrition Disorders/genetics/*metabolism ; Insulin/secretion ; Male ; Metabolic Diseases/metabolism ; Mice ; Mice, Inbred ICR ; Nucleosomes/metabolism ; Pregnancy ; *Prenatal Exposure Delayed Effects ; Spermatozoa/*metabolism/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Electronic Resource
    Electronic Resource
    Transgenes as molecular probes for genomic imprinting
    Amsterdam : Elsevier
    Trends in Genetics 4 (1988), S. 59-62 
    Details
    ISSN: 0168-9525
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0168-9525(88)90040-6
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  • 10
    Electronic Resource
    Electronic Resource
    Genomic imprinting and genetic disorders in man
    Amsterdam : Elsevier
    Trends in Genetics 5 (1989), S. 331-336 
    Details
    ISSN: 0168-9525
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0168-9525(89)90138-8
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