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Pesquisa : G02.111.570.080.708.330.800.200 [Categoria DeCS]
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[PMID]:28833526
[Au] Autor:Montrose L; Faulk C; Francis J; Dolinoy DC
[Ad] Endereço:Environmental Health Sciences, University of Michigan, Ann Arbor, Michigan.
[Ti] Título:Perinatal lead (Pb) exposure results in sex and tissue-dependent adult DNA methylation alterations in murine IAP transposons.
[So] Source:Environ Mol Mutagen;58(8):540-550, 2017 Oct.
[Is] ISSN:1098-2280
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidemiological and animal data suggest that adult chronic disease is influenced by early-life exposure-induced changes to the epigenome. Previously, we observed that perinatal lead (Pb) exposure results in persistent murine metabolic- and activity-related effects. Using phylogenetic and DNA methylation analysis, we have also identified novel intracisternal A particle (IAP) retrotransposons exhibiting regions of variable methylation as candidate loci for environmental effects on the epigenome. Here, we now evaluate brain and kidney DNA methylation profiles of four representative IAPs in adult mice exposed to human physiologically relevant levels of Pb two weeks prior to mating through lactation. When IAPs across the genome were evaluated globally, average (sd) methylation levels were 92.84% (3.74) differing by tissue (P < 0.001), but not sex or dose. By contrast, the four individual IAPs displayed tissue-specific Pb and sex effects. Medium Pb-exposed mice had 3.86% less brain methylation at IAP 110 (P < 0.01), while high Pb-exposed mice had 2.83% less brain methylation at IAP 236 (P = 0.01) and 1.77% less at IAP 506 (P = 0.05). Individual IAP DNA methylation differed by sex for IAP 110 in the brain and kidney, IAP 236 in the kidney, and IAP 1259 in the kidney. Using Tomtom, we identified three binding motifs that matched to each of our novel IAPs impacted by Pb, one of which (HMGA2) has been linked to metabolic-related conditions in both mice and humans. Thus, these recently identified IAPs display tissue-specific environmental lability as well as sex-specific differences supporting an epigenetic link between early exposure to Pb and later-in-life health outcomes. Environ. Mol. Mutagen. 58:540-550, 2017. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Metilação de DNA/efeitos dos fármacos
Elementos de DNA Transponíveis/genética
Genes de Partícula A Intracisternal/genética
Chumbo/toxicidade
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Encéfalo/crescimento & desenvolvimento
Elementos de DNA Transponíveis/efeitos dos fármacos
Epigenômica
Feminino
Genes de Partícula A Intracisternal/efeitos dos fármacos
Genoma
Seres Humanos
Rim/efeitos dos fármacos
Rim/crescimento & desenvolvimento
Camundongos
Filogenia
Gravidez
Efeitos Tardios da Exposição Pré-Natal
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA Transposable Elements); 2P299V784P (Lead)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1002/em.22119


  2 / 263 MEDLINE  
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[PMID]:27798843
[Au] Autor:Ramesh V; Bayam E; Cernilogar FM; Bonapace IM; Schulze M; Riemenschneider MJ; Schotta G; Götz M
[Ad] Endereço:Institute for Stem Cell Research, Helmholtz Center Munich, 85764 Neuherberg, Germany.
[Ti] Título:Loss of Uhrf1 in neural stem cells leads to activation of retroviral elements and delayed neurodegeneration.
[So] Source:Genes Dev;30(19):2199-2212, 2016 Oct 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In order to understand whether early epigenetic mechanisms instruct the long-term behavior of neural stem cells (NSCs) and their progeny, we examined Uhrf1 (ubiquitin-like PHD ring finger-1; also known as Np95), as it is highly expressed in NSCs of the developing brain and rapidly down-regulated upon differentiation. Conditional deletion of Uhrf1 in the developing cerebral cortex resulted in rather normal proliferation and neurogenesis but severe postnatal neurodegeneration. During development, deletion of Uhrf1 lead to global DNA hypomethylation with a strong activation of the intracisternal A particle (IAP) family of endogenous retroviral elements, accompanied by an increase in 5-hydroxymethylcytosine. Down-regulation of Tet enzymes rescued the IAP activation in Uhrf1 conditional knockout (cKO) cells, suggesting an antagonistic interplay between Uhrf1 and Tet on IAP regulation. As IAP up-regulation persists into postnatal stages in the Uhrf1 cKO mice, our data show the lack of means to repress IAPs in differentiating neurons that normally never express Uhrf1 The high load of viral proteins and other transcriptional deregulation ultimately led to postnatal neurodegeneration. Taken together, these data show that early developmental NSC factors can have long-term effects in neuronal differentiation and survival. Moreover, they highlight how specific the consequences of widespread changes in DNA methylation are for certain classes of retroviral elements.
[Mh] Termos MeSH primário: Córtex Cerebral/citologia
Córtex Cerebral/fisiopatologia
Genes de Partícula A Intracisternal/genética
Células-Tronco Neurais/fisiologia
Neurogênese/genética
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
[Mh] Termos MeSH secundário: 5-Metilcitosina/análogos & derivados
5-Metilcitosina/metabolismo
Animais
Sobrevivência Celular/genética
Córtex Cerebral/embriologia
Metilação de DNA
Deleção de Genes
Camundongos
Camundongos Knockout
Células-Tronco Neurais/citologia
Células-Tronco Neurais/virologia
Ativação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nuclear Proteins); 0 (Uhrf1 protein, mouse); 1123-95-1 (5-hydroxymethylcytosine); 6R795CQT4H (5-Methylcytosine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE


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[PMID]:27151458
[Au] Autor:Sharif J; Endo TA; Nakayama M; Karimi MM; Shimada M; Katsuyama K; Goyal P; Brind'Amour J; Sun MA; Sun Z; Ishikura T; Mizutani-Koseki Y; Ohara O; Shinkai Y; Nakanishi M; Xie H; Lorincz MC; Koseki H
[Ad] Endereço:Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences (IMS), 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
[Ti] Título:Activation of Endogenous Retroviruses in Dnmt1(-/-) ESCs Involves Disruption of SETDB1-Mediated Repression by NP95 Binding to Hemimethylated DNA.
[So] Source:Cell Stem Cell;19(1):81-94, 2016 Jul 07.
[Is] ISSN:1875-9777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Repression of endogenous retroviruses (ERVs) in mammals involves several epigenetic mechanisms. Acute loss of the maintenance methyltransferase Dnmt1 induces widespread DNA demethylation and transcriptional activation of ERVs, including CpG-rich IAP (intracisternal A particle) proviruses. Here, we show that this effect is not due simply to a loss of DNA methylation. Conditional deletions reveal that both Dnmt1 and Np95 are essential for maintenance DNA methylation. However, while IAPs are derepressed in Dnmt1-ablated embryos and embryonic stem cells (ESCs), these ERVs remain silenced when Np95 is deleted alone or in combination with Dnmt1. This paradoxical phenotype results from an ectopic interaction between NP95 and the H3K9 methyltransferase SETDB1. Normally, SETDB1 maintains silencing of IAPs, but in the absence of DNMT1, prolonged binding of NP95 to hemimethylated DNA transiently disrupts SETDB1-dependent H3K9me3 deposition. Thus, our observations reveal an unexpected antagonistic interplay between two repressive pathways involved in retroviral silencing in mammalian cells.
[Mh] Termos MeSH primário: DNA (Citosina-5-)-Metiltransferases/metabolismo
Metilação de DNA/genética
DNA/metabolismo
Retrovirus Endógenos/metabolismo
Histona-Lisina N-Metiltransferase/metabolismo
Células-Tronco Embrionárias Murinas/metabolismo
Proteínas Nucleares/metabolismo
Ativação Viral
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
DNA (Citosina-5-)-Metiltransferase 1
Feminino
Dosagem de Genes
Regulação da Expressão Gênica no Desenvolvimento
Inativação Gênica
Genes de Partícula A Intracisternal
Loci Gênicos
Histonas/metabolismo
Lisina/metabolismo
Camundongos
Camundongos Knockout
Modelos Biológicos
Mutação/genética
Proteínas Nucleares/química
Placenta/metabolismo
Gravidez
Ligação Proteica
Domínios Proteicos
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histones); 0 (Nuclear Proteins); 0 (Uhrf1 protein, mouse); 9007-49-2 (DNA); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.1.1.37 (Dnmt1 protein, mouse); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.1.1.43 (SETDB1 protein, mouse); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160507
[St] Status:MEDLINE


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[PMID]:26012739
[Au] Autor:Sadic D; Schmidt K; Groh S; Kondofersky I; Ellwart J; Fuchs C; Theis FJ; Schotta G
[Ad] Endereço:Adolf-Butenandt-Institute, Ludwig Maximilians University and Munich Center for Integrated Protein Science (CiPS), Munich, Germany.
[Ti] Título:Atrx promotes heterochromatin formation at retrotransposons.
[So] Source:EMBO Rep;16(7):836-50, 2015 Jul.
[Is] ISSN:1469-3178
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:More than 50% of mammalian genomes consist of retrotransposon sequences. Silencing of retrotransposons by heterochromatin is essential to ensure genomic stability and transcriptional integrity. Here, we identified a short sequence element in intracisternal A particle (IAP) retrotransposons that is sufficient to trigger heterochromatin formation. We used this sequence in a genome-wide shRNA screen and identified the chromatin remodeler Atrx as a novel regulator of IAP silencing. Atrx binds to IAP elements and is necessary for efficient heterochromatin formation. In addition, Atrx facilitates a robust and largely inaccessible heterochromatin structure as Atrx knockout cells display increased chromatin accessibility at retrotransposons and non-repetitive heterochromatic loci. In summary, we demonstrate a direct role of Atrx in the establishment and robust maintenance of heterochromatin.
[Mh] Termos MeSH primário: DNA Helicases/genética
DNA Helicases/metabolismo
Genes de Partícula A Intracisternal
Heterocromatina/metabolismo
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
[Mh] Termos MeSH secundário: Montagem e Desmontagem da Cromatina
Instabilidade Genômica
Heterocromatina/genética
Interferência de RNA
RNA Interferente Pequeno
Proteína Nuclear Ligada ao X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Heterochromatin); 0 (Nuclear Proteins); 0 (RNA, Small Interfering); EC 3.6.4.- (DNA Helicases); EC 3.6.4.12 (Atrx protein, mouse); EC 3.6.4.12 (X-linked Nuclear Protein)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150528
[St] Status:MEDLINE
[do] DOI:10.15252/embr.201439937


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[PMID]:25835743
[Au] Autor:Concepcion D; Ross KD; Hutt KR; Yeo GW; Hamilton BA
[Ad] Endereço:Department of Cellular and Molecular Medicine, Moores UCSD Cancer Center and Institute for Genomic Medicine, University of California, San Diego School of Medicine, La Jolla, California, United States of America; Department of Medicine, University of California, San Diego School of Medicine, La Joll
[Ti] Título:Nxf1 natural variant E610G is a semi-dominant suppressor of IAP-induced RNA processing defects.
[So] Source:PLoS Genet;11(4):e1005123, 2015 Apr.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endogenous retroviruses and retrotransposons contribute functional genetic variation in animal genomes. In mice, Intracisternal A Particles (IAPs) are a frequent source of both new mutations and polymorphism across laboratory strains. Intronic IAPs can induce alternative RNA processing choices, including alternative splicing. We previously showed IAP I∆1 subfamily insertional mutations are suppressed by a wild-derived allele of the major mRNA export factor, Nxf1. Here we show that a wider diversity of IAP insertions present in the mouse reference sequence induce insertion-dependent alternative processing that is suppressed by Nxf1CAST alleles. These insertions typically show more modest gene expression changes than de novo mutations, suggesting selection or attenuation. Genome-wide splicing-sensitive microarrays and gene-focused assays confirm specificity of Nxf1 genetic modifier activity for IAP insertion alleles. Strikingly, CRISPR/Cas9-mediated genome editing demonstrates that a single amino acid substitution in Nxf1, E610G, is sufficient to recreate a quantitative genetic modifier in a co-isogenic background.
[Mh] Termos MeSH primário: Genes de Partícula A Intracisternal
Genes Supressores
Mutação de Sentido Incorreto
Proteínas de Transporte Nucleocitoplasmático/metabolismo
Processamento de RNA
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Animais
Genes Dominantes
Camundongos
Camundongos Endogâmicos C57BL
Proteínas de Transporte Nucleocitoplasmático/genética
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (NXF1 protein, mouse); 0 (Nucleocytoplasmic Transport Proteins); 0 (RNA, Messenger)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150404
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1005123


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[PMID]:25257647
[Au] Autor:Juriloff DM; Harris MJ; Mager DL; Gagnier L
[Ad] Endereço:Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada.
[Ti] Título:Epigenetic mechanism causes Wnt9b deficiency and nonsyndromic cleft lip and palate in the A/WySn mouse strain.
[So] Source:Birth Defects Res A Clin Mol Teratol;100(10):772-88, 2014 Oct.
[Is] ISSN:1542-0760
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The heritable multifactorial etiology of human nonsyndromic cleft lip with or without cleft palate (CL ± P) is not understood. CL ± P occurs in 15% of neonates in the homozygous A/WySn mouse strain, with a multifactorial genetic etiology, the clf1 and clf2 variant genes. Clf1 acts as a mutant allele of Wnt9b but its coding sequence is normal. An IAP (intracisternal A particle) retrotransposon inserted near the Wnt9b gene is associated with clf1. METHODS: Transcription of noncoding sequence between the IAP and the Wnt9b gene was examined in A/WySn embryos. The levels of Wnt9b transcript and of an "IAP antisense" transcript initiated in the IAP and extending into the noncoding interval were assayed in A/WySn and C57BL/6J whole embryos or heads across embryonic days 8 to 12. Methylation of the 5' LTR of the IAP was examined in E12 A/WySn embryo heads. RESULTS: Mean Wnt9b transcript levels were lower in A/WySn than in C57BL/6J at all ages examined and lower in CL ± P embryos than in their normal littermates. The "IAP antisense" transcript was found in all A/WySn embryos and was highest in CL ± P embryos. The IAP at Wnt9b was generally unmethylated in CL ± P embryos and approximately 50% methylated in normal littermates. CONCLUSION: The clf1 mutation in A/WySn is a "metastable epiallele", in which stochastic deficiency in some individuals of DNA methylation of a retrotransposon uniquely inserted near the Wnt9b gene allows transcriptional activity of the retrotransposon and interference with transcription from Wnt9b. Methylation of metastable epialleles should be investigated in human nonsyndromic CL ± P.
[Mh] Termos MeSH primário: Fenda Labial/genética
Fissura Palatina/genética
Metilação de DNA/fisiologia
Embrião de Mamíferos/embriologia
Proteínas Wnt/deficiência
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Sequência de Bases
Metilação de DNA/genética
Embrião de Mamíferos/ultraestrutura
Genes de Partícula A Intracisternal/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Microscopia Eletrônica de Varredura
Dados de Sequência Molecular
Compostos Orgânicos
Reação em Cadeia da Polimerase em Tempo Real
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Organic Chemicals); 0 (Wnt Proteins); 0 (Wnt9b protein, mouse); 163795-75-3 (SYBR Green I)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140927
[St] Status:MEDLINE
[do] DOI:10.1002/bdra.23320


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[PMID]:25191835
[Au] Autor:Stathopoulou A; Lucchiari G; Ooi SK
[Ad] Endereço:Department of Cancer Biology, University College London Cancer Institute, London, United Kingdom.
[Ti] Título:DNA methylation is dispensable for suppression of the agouti viable yellow controlling element in murine embryonic stem cells.
[So] Source:PLoS One;9(9):e107355, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The agouti viable (Avy) locus is considered a model to understand how retroelements function as controlling elements in mammals. Epigenetic factors, principally CpG methylation, are widely held to play a dominant regulatory role in controlling the locus' activity. The purpose of this study was to examine its behavior in ES cells and determine if this locus could be exploited for use in screen-based investigations. We have derived multiple Avy ES cell lines from the C57BL/6 strain and generated a cell line carrying a GFP-reporter gene (Avy/AGFP). Use of the DNA demethylating drug 5-azacitidine on various ES cell lines does not induce either agouti or GFP expression. Methylation analysis reveals that although most lines display normal methylation at IAP elements in general, the Avy IAP element is essentially unmethylated. In addition, we find that different repeat compartments are epigenetically unstable in a number of derived cell lines.
[Mh] Termos MeSH primário: Proteína Agouti Sinalizadora/genética
Metilação de DNA
Células-Tronco Embrionárias/metabolismo
Sequências Reguladoras de Ácido Nucleico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Células Cultivadas
Regulação para Baixo/genética
Embrião de Mamíferos
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Genes de Partícula A Intracisternal/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Sequências Reguladoras de Ácido Nucleico/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Agouti Signaling Protein)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140906
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0107355


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[PMID]:25003790
[Au] Autor:Ekram MB; Kim J
[Ad] Endereço:Department of Biological Sciences, Louisiana State University, Baton Rouge, Louisiana, United States of America.
[Ti] Título:High-throughput targeted repeat element bisulfite sequencing (HT-TREBS): genome-wide DNA methylation analysis of IAP LTR retrotransposon.
[So] Source:PLoS One;9(7):e101683, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In vertebrates, DNA methylation-mediated repression of retrotransposons is essential for the maintenance of genomic integrity. In the current study, we developed a technique termed HT-TREBS (High-Throughput Targeted Repeat Element Bisulfite Sequencing). This technique is designed to measure the DNA methylation levels of individual loci of any repeat families with next-generation sequencing approaches. To test the feasibility of HT-TREBS, we analyzed the DNA methylation levels of the IAP LTR family using a set of 12 different genomic DNA isolated from the brain, liver and kidney of 4 one-week-old littermates of the mouse strain C57BL/6N. This technique has successfully generated the CpG methylation data of 5,233 loci common in all the samples, representing more than 80% of the individual loci of the five targeted subtypes of the IAP LTR family. According to the results, approximately 5% of the IAP LTR loci have less than 80% CpG methylation levels with no genomic position preference. Further analyses of the IAP LTR loci also revealed the presence of extensive DNA methylation variations between different tissues and individuals. Overall, these data demonstrate the efficiency and robustness of the new technique, HT-TREBS, and also provide new insights regarding the genome-wide DNA methylation patterns of the IAP LTR repeat elements.
[Mh] Termos MeSH primário: Metilação de DNA
Genes de Partícula A Intracisternal
Estudo de Associação Genômica Ampla/métodos
Sequenciamento de Nucleotídeos em Larga Escala/métodos
[Mh] Termos MeSH secundário: Animais
Biologia Computacional
Ilhas de CpG
Feminino
Masculino
Camundongos
Retroelementos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Retroelements)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140709
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0101683


  9 / 263 MEDLINE  
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[PMID]:24768537
[Au] Autor:Bierhoff H; Dammert MA; Brocks D; Dambacher S; Schotta G; Grummt I
[Ad] Endereço:Division of Molecular Biology of the Cell II, German Cancer Research Center, DKFZ-ZMBH Alliance, 69120 Heidelberg, Germany.
[Ti] Título:Quiescence-induced LncRNAs trigger H4K20 trimethylation and transcriptional silencing.
[So] Source:Mol Cell;54(4):675-82, 2014 May 22.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A complex network of regulatory pathways links transcription to cell growth and proliferation. Here we show that cellular quiescence alters chromatin structure by promoting trimethylation of histone H4 at lysine 20 (H4K20me3). In contrast to pericentric or telomeric regions, recruitment of the H4K20 methyltransferase Suv4-20h2 to rRNA genes and IAP elements requires neither trimethylation of H3K9 nor interaction with HP1 proteins but depends on long noncoding RNAs (lncRNAs) that interact with Suv4-20h2. Growth factor deprivation and terminal differentiation lead to upregulation of these lncRNAs, increase in H4K20me3, and chromatin compaction. The results uncover a lncRNA-mediated mechanism that guides Suv4-20h2 to specific genomic loci to establish a more compact chromatin structure in growth-arrested cells.
[Mh] Termos MeSH primário: Cromatina/metabolismo
Inativação Gênica
Genes de RNAr
Histona-Lisina N-Metiltransferase/metabolismo
Histonas/metabolismo
Lisina/metabolismo
RNA Longo não Codificante/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Cromatina/genética
Regulação da Expressão Gênica
Genes de Partícula A Intracisternal
Loci Gênicos
Histona-Lisina N-Metiltransferase/genética
Histonas/química
Histonas/genética
Metilação
Camundongos
Células NIH 3T3
RNA Longo não Codificante/genética
Telômero/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromatin); 0 (Histones); 0 (RNA, Long Noncoding); EC 2.1.1.125 (Suv4-20h protein, mouse); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:140526
[Lr] Data última revisão:
140526
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140429
[St] Status:MEDLINE


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[PMID]:24676381
[Au] Autor:Newman MR; Sykes PJ; Blyth BJ; Bezak E; Lawrence MD; Morel KL; Ormsby RJ
[Ad] Endereço:Flinders Centre for Innovation in Cancer, Flinders University and Medical Centre, Bedford Park, South Australia, Australia.
[Ti] Título:A single whole-body low dose X-irradiation does not affect L1, B1 and IAP repeat element DNA methylation longitudinally.
[So] Source:PLoS One;9(3):e93016, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The low dose radioadaptive response has been shown to be protective against high doses of radiation as well as aging-induced genomic instability. We hypothesised that a single whole-body exposure of low dose radiation would induce a radioadaptive response thereby reducing or abrogating aging-related changes in repeat element DNA methylation in mice. Following sham or 10 mGy X-irradiation, serial peripheral blood sampling was performed and differences in Long Interspersed Nucleic Element 1 (L1), B1 and Intracisternal-A-Particle (IAP) repeat element methylation between samples were assessed using high resolution melt analysis of PCR amplicons. By 420 days post-irradiation, neither radiation- or aging-related changes in the methylation of peripheral blood, spleen or liver L1, B1 and IAP elements were observed. Analysis of the spleen and liver tissues of cohorts of untreated aging mice showed that the 17-19 month age group exhibited higher repeat element methylation than younger or older mice, with no overall decline in methylation detected with age. This is the first temporal analysis of the effect of low dose radiation on repeat element methylation in mouse peripheral blood and the first to examine the long term effect of this dose on repeat element methylation in a radiosensitive tissue (spleen) and a tissue fundamental to the aging process (liver). Our data indicate that the methylation of murine DNA repeat elements can fluctuate with age, but unlike human studies, do not demonstrate an overall aging-related decline. Furthermore, our results indicate that a low dose of ionising radiation does not induce detectable changes to murine repeat element DNA methylation in the tissues and at the time-points examined in this study. This radiation dose is relevant to human diagnostic radiation exposures and suggests that a dose of 10 mGy X-rays, unlike high dose radiation, does not cause significant short or long term changes to repeat element or global DNA methylation.
[Mh] Termos MeSH primário: Metilação de DNA/efeitos da radiação
Genes de Partícula A Intracisternal/efeitos da radiação
Elementos Nucleotídeos Longos e Dispersos/efeitos da radiação
Dose de Radiação
Irradiação Corporal Total
Raios X
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Feminino
Fígado/metabolismo
Fígado/efeitos da radiação
Masculino
Camundongos
Modelos Animais
Sequências Repetitivas de Ácido Nucleico/efeitos da radiação
Baço/metabolismo
Baço/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140329
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0093016



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