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  • 1
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    Protein kinase C and regulation of the local competence of Xenopus ectoderm (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-01
    Description: The limited competence of embryonic tissue to respond to an inductive signal has an essential, regulatory function in embryonic induction. The molecular basis for the competence of Xenopus ectoderm to differentiate into neural tissue was investigated. Dorsal mesoderm or 12-O-tetradecanoyl phorbol-13-acetate (TPA) caused in vivo activation of protein kinase C (PKC) and neural differentiation mainly in dorsal ectoderm and to a lesser extent in ventral ectoderm. These data correlate with the observations that PKC preparations from dorsal and ventral ectoderm differ, the dorsal PKC preparation being more susceptible to activation by TPA and diolein than is the ventral PKC preparation. Monoclonal antibodies against the bovine PKC alpha plus beta or gamma isozymes immunostained dorsal and ventral ectoderm, respectively, which suggests different localizations of PKC isozymes. These results suggest that PKC participates in the establishment of embryonic competence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Otte, A P -- Kramer, I M -- Durston, A J -- New York, N.Y. -- Science. 1991 Feb 1;251(4993):570-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1990433" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Cell Differentiation ; Diglycerides/pharmacology ; Ectoderm/enzymology/*physiology ; Embryo, Nonmammalian/*physiology ; Enzyme Activation ; Isoenzymes/*metabolism ; Mesoderm/physiology ; Nervous System/embryology ; Protein Kinase C/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Xenopus
    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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    Epigenetic dynamics of imprinted X inactivation during early mouse development (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: The initiation of X-chromosome inactivation is thought to be tightly correlated with early differentiation events during mouse development. Here, we show that although initially active, the paternal X chromosome undergoes imprinted inactivation from the cleavage stages, well before cellular differentiation. A reversal of the inactive state, with a loss of epigenetic marks such as histone modifications and polycomb proteins, subsequently occurs in cells of the inner cell mass (ICM), which give rise to the embryo-proper in which random X inactivation is known to occur. This reveals the remarkable plasticity of the X-inactivation process during preimplantation development and underlines the importance of the ICM in global reprogramming of epigenetic marks in the early embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okamoto, Ikuhiro -- Otte, Arie P -- Allis, C David -- Reinberg, Danny -- Heard, Edith -- New York, N.Y. -- Science. 2004 Jan 30;303(5658):644-9. Epub 2003 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR218, Curie Institute, 26 rue d'Ulm, Paris 75005, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671313" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Blastocyst/physiology ; Blastomeres/physiology ; Chromatin/metabolism ; Chromosomes, Mammalian/physiology ; *Dosage Compensation, Genetic ; Embryo, Mammalian/*physiology ; *Embryonic and Fetal Development ; *Epigenesis, Genetic ; Female ; *Genomic Imprinting ; Histones/metabolism ; Male ; Methylation ; Mice ; Morula/physiology ; RNA, Long Noncoding ; RNA, Untranslated/metabolism ; Transcription, Genetic ; 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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  • 3
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    Role of histone H3 lysine 27 methylation in X inactivation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-22
    Description: The Polycomb group (PcG) protein Eed is implicated in regulation of imprinted X-chromosome inactivation in extraembryonic cells but not of random X inactivation in embryonic cells. The Drosophila homolog of the Eed-Ezh2 PcG protein complex achieves gene silencing through methylation of histone H3 on lysine 27 (H3-K27), which suggests a role for H3-K27 methylation in imprinted X inactivation. Here we demonstrate that transient recruitment of the Eed-Ezh2 complex to the inactive X chromosome (Xi) occurs during initiation of X inactivation in both extraembryonic and embryonic cells and is accompanied by H3-K27 methylation. Recruitment of the complex and methylation on the Xi depend on Xist RNA but are independent of its silencing function. Together, our results suggest a role for Eed-Ezh2-mediated H3-K27 methylation during initiation of both imprinted and random X inactivation and demonstrate that H3-K27 methylation is not sufficient for silencing of the Xi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plath, Kathrin -- Fang, Jia -- Mlynarczyk-Evans, Susanna K -- Cao, Ru -- Worringer, Kathleen A -- Wang, Hengbin -- de la Cruz, Cecile C -- Otte, Arie P -- Panning, Barbara -- Zhang, Yi -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):131-5. Epub 2003 Mar 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism/*physiology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; *Dosage Compensation, Genetic ; Female ; Fluorescent Antibody Technique ; Genomic Imprinting ; HeLa Cells ; Histones/*metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mutation ; Polycomb Repressive Complex 2 ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/metabolism ; Stem Cells/metabolism/*physiology ; Transgenes ; Trophoblasts/*physiology ; X Chromosome/*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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  • 4
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    Reactivation of the paternal X chromosome in early mouse embryos (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-31
    Description: It is generally accepted that paternally imprinted X inactivation occurs exclusively in extraembryonic lineages of mouse embryos, whereas cells of the embryo proper, derived from the inner cell mass (ICM), undergo only random X inactivation. Here we show that imprinted X inactivation, in fact, occurs in all cells of early embryos and that the paternal X is then selectively reactivated in cells allocated to the ICM. This contrasts with more differentiated cell types where X inactivation is highly stable and generally irreversible. Our observations illustrate that an important component of genome plasticity in early development is the capacity to reverse heritable gene silencing decisions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mak, Winifred -- Nesterova, Tatyana B -- de Napoles, Mariana -- Appanah, Ruth -- Yamanaka, Shinya -- Otte, Arie P -- Brockdorff, Neil -- New York, N.Y. -- Science. 2004 Jan 30;303(5658):666-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉X inactivation group, MRC Clinical Sciences Centre, ICSM, Hammersmith Hospital, London, W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14752160" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Blastocyst/physiology ; Cell Cycle Proteins/genetics/metabolism ; Chromosomal Proteins, Non-Histone/genetics/metabolism ; Chromosomes, Mammalian/physiology ; *Dosage Compensation, Genetic ; Embryo, Mammalian/*physiology ; Embryonic and Fetal Development ; Female ; *Gene Expression Regulation, Developmental ; Genomic Imprinting ; Histones/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Morula/physiology ; Polycomb Repressive Complex 2 ; Proteins/genetics/metabolism ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/genetics/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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  • 5
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    Akt-mediated phosphorylation of EZH2 suppresses methylation of lysine 27 in histone H3 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-15
    Description: Enhancer of Zeste homolog 2 (EZH2) is a methyltransferase that plays an important role in many biological processes through its ability to trimethylate lysine 27 in histone H3. Here, we show that Akt phosphorylates EZH2 at serine 21 and suppresses its methyltransferase activity by impeding EZH2 binding to histone H3, which results in a decrease of lysine 27 trimethylation and derepression of silenced genes. Our results imply that Akt regulates the methylation activity, through phosphorylation of EZH2, which may contribute to oncogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cha, Tai-Lung -- Zhou, Binhua P -- Xia, Weiya -- Wu, Yadi -- Yang, Cheng-Chieh -- Chen, Chun-Te -- Ping, Bo -- Otte, Arie P -- Hung, Mien-Chie -- P01 099031/PHS HHS/ -- R01 109311/PHS HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):306-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, the University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224021" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; COS Cells ; Cell Line ; Cell Transformation, Neoplastic ; Cercopithecus aethiops ; Chromones/pharmacology ; DNA-Binding Proteins ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation ; HeLa Cells ; Histone-Lysine N-Methyltransferase/metabolism ; Histones/*metabolism ; Homeodomain Proteins/genetics ; Humans ; Lysine/*metabolism ; Methylation ; Mice ; Molecular Sequence Data ; Morpholines/pharmacology ; Phosphorylation ; Polycomb Repressive Complex 2 ; Protein Binding ; Protein Methyltransferases ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/*metabolism ; Proteins/*metabolism ; Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins c-akt ; Serine/metabolism ; Transcription Factors
    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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  • 6
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    Impeding Xist expression from the active X chromosome improves mouse somatic cell nuclear transfer (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-18
    Description: Cloning mammals by means of somatic cell nuclear transfer (SCNT) is highly inefficient because of erroneous reprogramming of the donor genome. Reprogramming errors appear to arise randomly, but the nature of nonrandom, SCNT-specific errors remains elusive. We found that Xist, a noncoding RNA that inactivates one of the two X chromosomes in females, was ectopically expressed from the active X (Xa) chromosome in cloned mouse embryos of both sexes. Deletion of Xist on Xa showed normal global gene expression and resulted in about an eight- to ninefold increase in cloning efficiency. We also identified an Xist-independent mechanism that specifically down-regulated a subset of X-linked genes through somatic-type repressive histone blocks. Thus, we have identified nonrandom reprogramming errors in mouse cloning that can be altered to improve the efficiency of SCNT methods.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inoue, Kimiko -- Kohda, Takashi -- Sugimoto, Michihiko -- Sado, Takashi -- Ogonuki, Narumi -- Matoba, Shogo -- Shiura, Hirosuke -- Ikeda, Rieko -- Mochida, Keiji -- Fujii, Takashi -- Sawai, Ken -- Otte, Arie P -- Tian, X Cindy -- Yang, Xiangzhong -- Ishino, Fumitoshi -- Abe, Kuniya -- Ogura, Atsuo -- New York, N.Y. -- Science. 2010 Oct 22;330(6003):496-9. doi: 10.1126/science.1194174. Epub 2010 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BioResource Center, RIKEN, 305-0024 Tsukuba, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847234" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Organism/*methods ; Down-Regulation ; Embryo, Mammalian/metabolism ; Female ; Gene Deletion ; Gene Expression Profiling ; Male ; Mice ; *Nuclear Transfer Techniques ; RNA, Long Noncoding ; RNA, Untranslated/biosynthesis/genetics/*physiology ; *X Chromosome
    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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