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  • 1
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    Regulation of maternal behavior and offspring growth by paternally expressed Peg3 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: Imprinted genes display parent-of-origin-dependent monoallelic expression that apparently regulates complex mammalian traits, including growth and behavior. The Peg3 gene is expressed in embryos and the adult brain from the paternal allele only. A mutation in the Peg3 gene resulted in growth retardation, as well as a striking impairment of maternal behavior that frequently resulted in death of the offspring. This result may be partly due to defective neuronal connectivity, as well as reduced oxytocin neurons in the hypothalamus, because mutant mothers were deficient in milk ejection. This study provides further insights on the evolution of epigenetic regulation of imprinted gene dosage in modulating mammalian growth and behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, L -- Keverne, E B -- Aparicio, S A -- Ishino, F -- Barton, S C -- Surani, M A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):330-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome CRC Institute of Cancer and Developmental Biology, and Physiological Laboratory, 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/10195900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/metabolism ; Crosses, Genetic ; Female ; Gene Expression ; Gene Targeting ; *Genomic Imprinting ; *Growth ; Hypothalamus/cytology/metabolism ; Kruppel-Like Transcription Factors ; Lactation ; Male ; *Maternal Behavior ; Mice ; Mutation ; Neural Pathways ; Neurons/metabolism ; Oxytocin/metabolism ; Phenotype ; *Protein Kinases ; Proteins/genetics/*physiology ; *Transcription Factors ; *Weight Gain
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Imprinting and the epigenetic asymmetry between parental genomes (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-11
    Description: Genomic imprinting confers a developmental asymmetry on the parental genomes, through epigenetic modifications in the germ line and embryo. These heritable modifications regulate the monoallelic activity of parental alleles resulting in their functional differences during development. Specific cis-acting regulatory elements associated with imprinted genes carry modifications involving chromatin structural changes and DNA methylation. Some of these modifications are initiated in the germ line. Comparative genomic analysis at imprinted domains is emerging as a powerful tool for the identification of conserved elements amenable to more detailed functional analysis, and for providing insight into the emergence of imprinting during the evolution of mammalian species. Genomic imprinting therefore provides a model system for the analysis of the epigenetic control of genome function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferguson-Smith, A C -- Surani, M A -- New York, N.Y. -- Science. 2001 Aug 10;293(5532):1086-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of Cambridge, Downing Street, Cambridge, CB2 3DY, UK. afsmith@mole.bio.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11498578" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; DNA Methylation ; Embryonic and Fetal Development ; Evolution, Molecular ; Female ; Gametogenesis ; *Gene Expression Regulation, Developmental ; Gene Silencing ; *Genomic Imprinting ; Germ Cells/*metabolism ; Humans ; Male ; Oocytes/metabolism ; RNA, Antisense/genetics ; Regulatory Sequences, Nucleic Acid ; Zygote/metabolism
    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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  • 3
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    Endogenous siRNAs from naturally formed dsRNAs regulate transcripts in mouse oocytes (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-12
    Description: RNA interference (RNAi) is a mechanism by which double-stranded RNAs (dsRNAs) suppress specific transcripts in a sequence-dependent manner. dsRNAs are processed by Dicer to 21-24-nucleotide small interfering RNAs (siRNAs) and then incorporated into the argonaute (Ago) proteins. Gene regulation by endogenous siRNAs has been observed only in organisms possessing RNA-dependent RNA polymerase (RdRP). In mammals, where no RdRP activity has been found, biogenesis and function of endogenous siRNAs remain largely unknown. Here we show, using mouse oocytes, that endogenous siRNAs are derived from naturally occurring dsRNAs and have roles in the regulation of gene expression. By means of deep sequencing, we identify a large number of both approximately 25-27-nucleotide Piwi-interacting RNAs (piRNAs) and approximately 21-nucleotide siRNAs corresponding to messenger RNAs or retrotransposons in growing oocytes. piRNAs are bound to Mili and have a role in the regulation of retrotransposons. siRNAs are exclusively mapped to retrotransposons or other genomic regions that produce transcripts capable of forming dsRNA structures. Inverted repeat structures, bidirectional transcription and antisense transcripts from various loci are sources of the dsRNAs. Some precursor transcripts of siRNAs are derived from expressed pseudogenes, indicating that one role of pseudogenes is to adjust the level of the founding source mRNA through RNAi. Loss of Dicer or Ago2 results in decreased levels of siRNAs and increased levels of retrotransposon and protein-coding transcripts complementary to the siRNAs. Thus, the RNAi pathway regulates both protein-coding transcripts and retrotransposons in mouse oocytes. Our results reveal a role for endogenous siRNAs in mammalian oocytes and show that organisms lacking RdRP activity can produce functional endogenous siRNAs from naturally occurring dsRNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watanabe, Toshiaki -- Totoki, Yasushi -- Toyoda, Atsushi -- Kaneda, Masahiro -- Kuramochi-Miyagawa, Satomi -- Obata, Yayoi -- Chiba, Hatsune -- Kohara, Yuji -- Kono, Tomohiro -- Nakano, Toru -- Surani, M Azim -- Sakaki, Yoshiyuki -- Sasaki, Hiroyuki -- England -- Nature. 2008 May 22;453(7194):539-43. doi: 10.1038/nature06908. Epub 2008 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Genetics, Department of Integrated Genetics, National Institute of Genetics, Research Organization of Information and Systems, Mishima 411-8540, Japan. toshwata@lab.nig.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18404146" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Eukaryotic Initiation Factor-2/deficiency/genetics/metabolism ; Female ; Gene Expression Regulation, Developmental ; Gene Library ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Oocytes/growth & development/*metabolism ; Polymerase Chain Reaction ; Pseudogenes/genetics ; *RNA Interference ; RNA, Double-Stranded/*genetics/*metabolism ; RNA, Messenger/*genetics/metabolism ; RNA, Small Interfering/*genetics/*metabolism ; Retroelements/genetics ; Ribonuclease III/deficiency/genetics/metabolism
    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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  • 4
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    Chromatin dynamics during epigenetic reprogramming in the mouse germ line (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-03-21
    Description: A unique feature of the germ cell lineage is the generation of totipotency. A critical event in this context is DNA demethylation and the erasure of parental imprints in mouse primordial germ cells (PGCs) on embryonic day 11.5 (E11.5) after they enter into the developing gonads. Little is yet known about the mechanism involved, except that it is apparently an active process. We have examined the associated changes in the chromatin to gain further insights into this reprogramming event. Here we show that the chromatin changes occur in two steps. The first changes in nascent PGCs at E8.5 establish a distinctive chromatin signature that is reminiscent of pluripotency. Next, when PGCs are residing in the gonads, major changes occur in nuclear architecture accompanied by an extensive erasure of several histone modifications and exchange of histone variants. Furthermore, the histone chaperones HIRA and NAP-1 (NAP111), which are implicated in histone exchange, accumulate in PGC nuclei undergoing reprogramming. We therefore suggest that the mechanism of histone replacement is critical for these chromatin rearrangements to occur. The marked chromatin changes are intimately linked with genome-wide DNA demethylation. On the basis of the timing of the observed events, we propose that if DNA demethylation entails a DNA repair-based mechanism, the evident histone replacement would represent a repair-induced response event rather than being a prerequisite.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847605/" 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/PMC3847605/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hajkova, Petra -- Ancelin, Katia -- Waldmann, Tanja -- Lacoste, Nicolas -- Lange, Ulrike C -- Cesari, Francesca -- Lee, Caroline -- Almouzni, Genevieve -- Schneider, Robert -- Surani, M Azim -- 083089/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Apr 17;452(7189):877-81. doi: 10.1038/nature06714. Epub 2008 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust/Cancer Research UK Gurdon Institute of Cancer and Developmental Biology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18354397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/*metabolism ; *Chromatin Assembly and Disassembly ; DNA Methylation ; *Epigenesis, Genetic ; Germ Cells/*metabolism ; Gonads/cytology/metabolism ; Histones/metabolism ; Mice ; Stem Cells/metabolism
    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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    Epigenetic reversion of post-implantation epiblast to pluripotent embryonic stem cells (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-10-10
    Description: The pluripotent state, which is first established in the primitive ectoderm cells of blastocysts, is lost progressively and irreversibly during subsequent development. For example, development of post-implantation epiblast cells from primitive ectoderm involves significant transcriptional and epigenetic changes, including DNA methylation and X chromosome inactivation, which create a robust epigenetic barrier and prevent their reversion to a primitive-ectoderm-like state. Epiblast cells are refractory to leukaemia inhibitory factor (LIF)-STAT3 signalling, but they respond to activin/basic fibroblast growth factor to form self-renewing epiblast stem cells (EpiSCs), which exhibit essential properties of epiblast cells and that differ from embryonic stem (ES) cells derived from primitive ectoderm. Here we show reprogramming of advanced epiblast cells from embryonic day 5.5-7.5 mouse embryos with uniform expression of N-cadherin and inactive X chromosome to ES-cell-like cells (rESCs) in response to LIF-STAT3 signalling. Cultured epiblast cells overcome the epigenetic barrier progressively as they proceed with the erasure of key properties of epiblast cells, resulting in DNA demethylation, X reactivation and expression of E-cadherin. The accompanying changes in the transcriptome result in a loss of phenotypic and epigenetic memory of epiblast cells. Using this approach, we report reversion of established EpiSCs to rESCs. Moreover, unlike epiblast and EpiSCs, rESCs contribute to somatic tissues and germ cells in chimaeras. Further studies may reveal how signalling-induced epigenetic reprogramming may promote reacquisition of pluripotency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863718/" 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/PMC3863718/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bao, Siqin -- Tang, Fuchou -- Li, Xihe -- Hayashi, Katsuhiko -- Gillich, Astrid -- Lao, Kaiqin -- Surani, M Azim -- 083089/Wellcome Trust/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2009 Oct 29;461(7268):1292-5. doi: 10.1038/nature08534.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19816418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/metabolism ; Cadherins/metabolism ; Cells, Cultured ; Cellular Reprogramming ; DNA Methylation ; Ectoderm/cytology ; Embryo, Mammalian/cytology ; *Embryonic Development ; Embryonic Stem Cells/*cytology/*metabolism ; *Epigenesis, Genetic ; Gene Expression Profiling ; Germ Layers/*cytology/metabolism ; Leukemia Inhibitory Factor/metabolism ; Mice ; Pluripotent Stem Cells/*cytology/*metabolism ; STAT3 Transcription Factor/metabolism ; Y Chromosome/genetics
    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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    A role for Lin28 in primordial germ-cell development and germ-cell malignancy (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-07
    Description: The rarity and inaccessibility of the earliest primordial germ cells (PGCs) in the mouse embryo thwart efforts to investigate molecular mechanisms of germ-cell specification. stella (also called Dppa3) marks the rare founder population of the germ lineage. Here we differentiate mouse embryonic stem cells carrying a stella transgenic reporter into putative PGCs in vitro. The Stella(+) cells possess a transcriptional profile similar to embryo-derived PGCs, and like their counterparts in vivo, lose imprints in a time-dependent manner. Using inhibitory RNAs to screen candidate genes for effects on the development of Stella(+) cells in vitro, we discovered that Lin28, a negative regulator of let-7 microRNA processing, is essential for proper PGC development. Furthermore, we show that Blimp1 (also called Prdm1), a let-7 target and a master regulator of PGC specification, can rescue the effect of Lin28 deficiency during PGC development, thereby establishing a mechanism of action for Lin28 during PGC specification. Overexpression of Lin28 promotes formation of Stella(+) cells in vitro and PGCs in chimaeric embryos, and is associated with human germ-cell tumours. The differentiation of putative PGCs from embryonic stem cells in vitro recapitulates the early stages of gamete development in vivo, and provides an accessible system for discovering novel genes involved in germ-cell development and malignancy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729657/" 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/PMC2729657/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, Jason A -- Viswanathan, Srinivas R -- Yabuuchi, Akiko -- Cunniff, Kerianne -- Takeuchi, Ayumu -- Park, In-Hyun -- Sero, Julia E -- Zhu, Hao -- Perez-Atayde, Antonio -- Frazier, A Lindsay -- Surani, M Azim -- Daley, George Q -- DP1 OD000256/OD/NIH HHS/ -- DP1 OD000256-01/OD/NIH HHS/ -- G0300723/Medical Research Council/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- T32 CA009172/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Aug 13;460(7257):909-13. doi: 10.1038/nature08210. Epub 2009 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Hematology/Oncology, Children's Hospital Boston and the Dana-Farber Cancer Institute, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19578360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Line ; Embryonic Stem Cells/cytology/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Germ Cells/*cytology/*metabolism/pathology ; Humans ; Mice ; Mice, Inbred C57BL ; Neoplasms, Germ Cell and Embryonal/genetics/*metabolism/*pathology ; RNA-Binding Proteins/genetics/*metabolism ; Repressor Proteins/genetics/metabolism ; Transcription Factors/metabolism ; Transgenes
    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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    Germline DNA demethylation dynamics and imprint erasure through 5-hydroxymethylcytosine (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-12
    Description: Mouse primordial germ cells (PGCs) undergo sequential epigenetic changes and genome-wide DNA demethylation to reset the epigenome for totipotency. Here, we demonstrate that erasure of CpG methylation (5mC) in PGCs occurs via conversion to 5-hydroxymethylcytosine (5hmC), driven by high levels of TET1 and TET2. Global conversion to 5hmC initiates asynchronously among PGCs at embryonic day (E) 9.5 to E10.5 and accounts for the unique process of imprint erasure. Mechanistically, 5hmC enrichment is followed by its protracted decline thereafter at a rate consistent with replication-coupled dilution. The conversion to 5hmC is an important component of parallel redundant systems that drive comprehensive reprogramming in PGCs. Nonetheless, we identify rare regulatory elements that escape systematic DNA demethylation in PGCs, providing a potential mechanistic basis for transgenerational epigenetic inheritance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847602/" 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/PMC3847602/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hackett, Jamie A -- Sengupta, Roopsha -- Zylicz, Jan J -- Murakami, Kazuhiro -- Lee, Caroline -- Down, Thomas A -- Surani, M Azim -- 079249/Wellcome Trust/United Kingdom -- 083089/Wellcome Trust/United Kingdom -- 083563/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- RG44593/Wellcome Trust/United Kingdom -- RG49135/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2013 Jan 25;339(6118):448-52. doi: 10.1126/science.1229277. Epub 2012 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23223451" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Animals ; CpG Islands ; Cytosine/*analogs & derivatives/metabolism ; *DNA Methylation ; DNA-Binding Proteins/genetics/metabolism ; Embryo, Mammalian/*metabolism ; Embryonic Development ; *Epigenesis, Genetic ; Female ; *Genomic Imprinting ; Germ Cells/*metabolism ; Germ Layers/cytology ; Male ; Mice ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics/metabolism ; RNA-Binding Proteins/genetics
    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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    Development. Programming the X chromosome (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hajkova, Petra -- Surani, M Azim -- New York, N.Y. -- Science. 2004 Jan 30;303(5658):633-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge CB2 1QR, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14752149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Mammalian/physiology ; *Dosage Compensation, Genetic ; Embryo, Mammalian/*physiology ; *Embryo, Nonmammalian ; *Embryonic and Fetal Development ; Female ; *Gene Expression Regulation, Developmental ; Genes, Homeobox ; Genomic Imprinting ; Histones/metabolism ; Male ; Methylation ; Placenta/*physiology ; Pluripotent Stem Cells/physiology ; Polycomb Repressive Complex 2 ; Proteins/metabolism ; RNA, Long Noncoding ; RNA, Untranslated/metabolism ; Repressor Proteins/metabolism ; X Chromosome/*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
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    Germ cell specification in mice (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-21
    Description: Specification of germ cells in mice occurs relatively late in embryonic development. It is initiated by signals that induce expression of Blimp1, a key regulator of the germ cell, in a few epiblast cells of early postimplantation embryos. Blimp1 represses the incipient somatic program in these cells and promotes progression toward the germ cell fate. Blimp1 may also have a role in the maintenance of early germ cell characteristics by ensuring their escape from the somatic fate as well as possible reversion to pluripotent stem cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayashi, Katsuhiko -- de Sousa Lopes, Susana M Chuva -- Surani, M Azim -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):394-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446386" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Embryo, Mammalian/*cytology/physiology ; Embryonic Development ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Germ Cells/*cytology ; Mice ; Phenotype ; Pluripotent Stem Cells/cytology ; Protein Methyltransferases/genetics/physiology ; Repressor Proteins/physiology ; Transcription Factors/physiology ; Transcription, Genetic
    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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  • 10
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    Genome-wide reprogramming in the mouse germ line entails the base excision repair pathway (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-03
    Description: Genome-wide active DNA demethylation in primordial germ cells (PGCs), which reprograms the epigenome for totipotency, is linked to changes in nuclear architecture, loss of histone modifications, and widespread histone replacement. Here, we show that DNA demethylation in the mouse PGCs is mechanistically linked to the appearance of single-stranded DNA (ssDNA) breaks and the activation of the base excision repair (BER) pathway, as is the case in the zygote where the paternal pronucleus undergoes active DNA demethylation shortly after fertilization. Whereas BER might be triggered by deamination of a methylcytosine (5mC), cumulative evidence indicates other mechanisms in germ cells. We demonstrate that DNA repair through BER represents a core component of genome-wide DNA demethylation in vivo and provides a mechanistic link to the extensive chromatin remodeling in developing PGCs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3863715/" 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/PMC3863715/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hajkova, Petra -- Jeffries, Sean J -- Lee, Caroline -- Miller, Nigel -- Jackson, Stephen P -- Surani, M Azim -- 083089/Wellcome Trust/United Kingdom -- 11224/Cancer Research UK/United Kingdom -- A11224/Cancer Research UK/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- MC_U120092689/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):78-82. doi: 10.1126/science.1187945.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust-Cancer Research U.K. Gurdon Institute of Cancer and Developmental Biology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK. petra.hajkova@csc.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Cell Nucleus/metabolism ; Chromatin/metabolism ; *Chromatin Assembly and Disassembly ; *DNA Breaks, Single-Stranded ; *DNA Methylation ; *DNA Repair/drug effects ; DNA-Binding Proteins/metabolism ; Embryo, Mammalian/metabolism ; Embryonic Development ; Enzyme Inhibitors/pharmacology ; *Epigenesis, Genetic ; Female ; *Genome ; Germ Cells/*metabolism ; Histones/metabolism ; Indoles/pharmacology ; Male ; Mice ; Poly Adenosine Diphosphate Ribose/metabolism ; Zygote/drug effects/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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