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Placental-specific IGF-II is a major modulator of placental and fetal growth
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As for Ipl and Ascl2 [9,48], the expression of Igf2 is important for the development and function of the placenta. Deletion of one of the Igf2 promoters, transcribed in the labyrinthine trophoblast, was found to give rise to a comparable growth-deficiency as resulting from the complete abolishment of Igf2 expression. This work emphasises the importance of imprinting for placental development.
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Constância M., Hemberger M., Hughes J., Dean W., Ferguson-Smith A., Fundele R., Stewart F., Kelsey G., Fowden A., Sibley C.et al. Placental-specific IGF-II is a major modulator of placental and fetal growth. Nature. 417:2002;945-948 As for Ipl and Ascl2 [9,48], the expression of Igf2 is important for the development and function of the placenta. Deletion of one of the Igf2 promoters, transcribed in the labyrinthine trophoblast, was found to give rise to a comparable growth-deficiency as resulting from the complete abolishment of Igf2 expression. This work emphasises the importance of imprinting for placental development.
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Constância, M.1
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Frank D., Fortino W., Clark L., Musalo R., Wang W., Saxena A., Li C.M., Reik W., Ludwig T., Tycko B. Placental overgrowth in mice lacking the imprinted gene Ipl. Proc Natl Acad Sci USA. 99:2002;7490-7495.
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Asymmetric regulation of imprinting on the maternal and paternal chromosomes at the Dlk1-Gtl2 imprinted cluster on mouse chromosome 12
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On mouse chromosome 12, there is a 1Mb imprinted cluster comprising the paternally-expressed protein-encoding genes Dlk1 and Dio3, and several maternally expressed non-coding RNAs (Gtl2, snoRNAs and microRNAs). In this study, a differentially methylated ICR was shown to regulate the levels of expression of all the genes of the cluster on the maternal chromosome.
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Lin S., Youngson N., Takada S., Seitz H., Reik W., Paulsen M., Cavaillé J., Ferguson-Smith A.C. Asymmetric regulation of imprinting on the maternal and paternal chromosomes at the Dlk1-Gtl2 imprinted cluster on mouse chromosome 12. Nat Genet. 35:2003;97-102 On mouse chromosome 12, there is a 1Mb imprinted cluster comprising the paternally-expressed protein-encoding genes Dlk1 and Dio3, and several maternally expressed non-coding RNAs (Gtl2, snoRNAs and microRNAs). In this study, a differentially methylated ICR was shown to regulate the levels of expression of all the genes of the cluster on the maternal chromosome.
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Lin, S.1
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Bourc'his D., Xu G.-L., Lin C.-S., Bollman B., Bestor T.H. Dnmt3L and the establishment of maternal genomic imprints. Science. 294:2001;2536-2539.
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Dnmt3L cooperates with the Dnmt3 family of de novo DNA methyltransferases to establish maternal imprints in mice
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Together with other work [12,14], this study establishes that Dnmt3l is essential for the establishment of maternal methylation imprints. This Dnmt-like protein has no enzymatic activity, but was found to co-localise with Dnmt3a and Dnmt3b in the nucleus. Gene-targeting studies are presented which indicate that Dnmt3l interacts with this/these de novo DNMTs to establish the maternal methylation imprints.
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Hata K., Okano M., Lei H., Li E. Dnmt3L cooperates with the Dnmt3 family of de novo DNA methyltransferases to establish maternal imprints in mice. Development. 129:2002;1983-1993 Together with other work [12,14], this study establishes that Dnmt3l is essential for the establishment of maternal methylation imprints. This Dnmt-like protein has no enzymatic activity, but was found to co-localise with Dnmt3a and Dnmt3b in the nucleus. Gene-targeting studies are presented which indicate that Dnmt3l interacts with this/these de novo DNMTs to establish the maternal methylation imprints.
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Hata, K.1
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Chédin F., Lieber M.R., Hsieh C. The DNA methyltransferase-like protein Dnmt3L stimulates de novo methylation by Dnmt3a. Proc Natl Acad Sci USA. 99:2002;16916-16921.
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Schoenherr C.J., Levorse J.M., Tilghman S.M. CTCF maintains differential methylation at the Igf2/H19 locus. Nat Genet. 33:2003;66-69.
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The nucleotides responsible for the direct physical contact between the chromatin insulator protein CTCF and the H19 imprinting control region manifest parent of origin-specific long-distance insulation and methylation-free domains
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Pant V., Mariano P., Kanduri C., Mattsson A., Lobanenkov V., Heuchel R., Ohlsson R. The nucleotides responsible for the direct physical contact between the chromatin insulator protein CTCF and the H19 imprinting control region manifest parent of origin-specific long-distance insulation and methylation-free domains. Genes Dev. 17:2003;586-590.
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Transgenic RNAi reveals essential function for CTCF in H19 imprinting
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To prevent the maternal allele of the ICR at the Igf2/H19 domain from becoming methylated, its CTCF binding sites are essential, at least in the embryo [15,16]. In this study, a transgenic RNAi approach was used to specifically downregulate CTCF expression during oogenesis. The data presented indicate that CTCF protects the ICR against becoming methylated in the female germ line too.
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Fedoriw A.M., Stein P., Svoboda P., Schultz R., Bartolomei M.S. Transgenic RNAi reveals essential function for CTCF in H19 imprinting. Science. 303:2004;238-240 To prevent the maternal allele of the ICR at the Igf2/H19 domain from becoming methylated, its CTCF binding sites are essential, at least in the embryo [15,16]. In this study, a transgenic RNAi approach was used to specifically downregulate CTCF expression during oogenesis. The data presented indicate that CTCF protects the ICR against becoming methylated in the female germ line too.
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Science
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Fedoriw, A.M.1
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Bowman A.B., Levorse J.M., Ingram R.S., Tilghman S.M. Functional characterization of a testis-specific DNA binding activity at the H19/Igf2 imprinting control region. Mol Cell Biol. 23:2003;8345-8351.
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Zwart R., Sleutels F., Wutz A., Schinkel A.H., Barlow D.P. Bidirectional action of the Igf2r imprint control element on upstream and downstream imprinted genes. Genes Dev. 15:2001;2361-2366.
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The non-coding Air RNA is required for silencing autosomal imprinted genes
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The mouse Igf2r imprinting cluster comprises several genes - Igf2r, Slc22a2, and Slc22a3 - that are repressed on the paternal chromosome. The intronic ICR in the Igf2r gene is essential for this paternal repression [19]. The ICR comprises the promoter for a paternally-expressed non-coding RNA, called Air. By introducing a premature poly-adenylation signal, leading to a truncated Air transcript, the authors show that this non-coding RNA is important for the silencing of the Igf2r, Slc22a2, and Slc22a3 genes on the paternal chromosome.
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Sleutels F., Zwart R., Barlow D.P. The non-coding Air RNA is required for silencing autosomal imprinted genes. Nature. 415:2002;810-813 The mouse Igf2r imprinting cluster comprises several genes - Igf2r, Slc22a2, and Slc22a3 - that are repressed on the paternal chromosome. The intronic ICR in the Igf2r gene is essential for this paternal repression [19]. The ICR comprises the promoter for a paternally-expressed non-coding RNA, called Air. By introducing a premature poly-adenylation signal, leading to a truncated Air transcript, the authors show that this non-coding RNA is important for the silencing of the Igf2r, Slc22a2, and Slc22a3 genes on the paternal chromosome.
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Nature
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Sleutels, F.1
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Regulation of DNA methylation of Rasgrf1
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The mouse Rasgrf1 locus has a paternally methylated region located 30kb upstream of Rasgrf1 - which is expressed from the paternal allele only in neonatal brain. This work establishes that the differential DNA methylation is regulated by a close-by repeated sequence (a 41-mer repeated 40 times). In addition, it is shown that the paternal allele-specific methylation is essential for the imprinted Rasgrf1 expression.
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Yoon B.J., Herman H., Sikora A., Smith L.T., Plass C., Soloway P.D. Regulation of DNA methylation of Rasgrf1. Nat Genet. 30:2002;92-96 The mouse Rasgrf1 locus has a paternally methylated region located 30kb upstream of Rasgrf1 - which is expressed from the paternal allele only in neonatal brain. This work establishes that the differential DNA methylation is regulated by a close-by repeated sequence (a 41-mer repeated 40 times). In addition, it is shown that the paternal allele-specific methylation is essential for the imprinted Rasgrf1 expression.
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Yoon, B.J.1
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Herman H., Lu M., Anggraini M., Sikora A., Chang Y., Yoon B.J., Soloway P.D. Trans allele methylation and paramutation-like effects in mice. Nat Genet. 34:2003;199-202.
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Conserved methylation imprints in the human and mouse GRB10 genes with divergent allelic expression suggests differential reading of the same mark
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Arnaud P., Monk D., Hitchins M., Gordon E., Dean W., Beechey C.V., Peters J., Craigen W., Preece M., Stanier P.et al. Conserved methylation imprints in the human and mouse GRB10 genes with divergent allelic expression suggests differential reading of the same mark. Hum Mol Genet. 12:2003;1005-1019.
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Arnaud, P.1
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Hikichi T., Kohda T., Kaneko-Ishino T., Ishino F. Imprinting regulation of the murine Meg1/Grb10 and human GRB10 genes; roles of brain-specific promoters and mouse-specific CTCF-binding sites. Nucleic Acids Res. 31:2003;1398-1406.
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Epimutations in Prader-Willi and Angelman syndromes: A molecular study of 136 patients with an imprinting defect
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Buiting K., Gross S., Lich C., Gillessen-Kaesbach G., El-Maarri O., Horsthemke B. Epimutations in Prader-Willi and Angelman syndromes: a molecular study of 136 patients with an imprinting defect. Am J Hum Genet. 72:2003;571-577.
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The imprinting mechanism of the Prader-Willi/Angelman regional control center
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•], this work demonstrates that nearby sequence can influence the germ-line establishment of DNA methylation at ICRs.
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•], this work demonstrates that nearby sequence can influence the germ-line establishment of DNA methylation at ICRs.
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Perk, J.1
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Methylation imprints of the imprint control region of the SNRPN-gene in human gametes and preimplantation embryos
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Geuns E., De Rycke M., Van Steirteghem A., Liebaers I. Methylation imprints of the imprint control region of the SNRPN-gene in human gametes and preimplantation embryos. Hum Mol Genet. 12:2003;2873-2879.
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•] comprises microRNA genes that are expressed from the maternal chromosome only. These microRNAs are antisense to a retrotransposon-like gene expressed from the paternal allele.
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•] comprises microRNA genes that are expressed from the maternal chromosome only. These microRNAs are antisense to a retrotransposon-like gene expressed from the paternal allele.
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Seitz, H.1
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31
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Loss of IGF2 imprinting: A potential marker of colorectal cancer risk
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Cui H., Cruz-Correa M., Giardiello F.M., Hutcheon D.F., Kafonek D.R., Brandenburg S., Wu Y., He X., Powe N.R., Feinberg A.P. Loss of IGF2 imprinting: a potential marker of colorectal cancer risk. Science. 299:2003;1753-1755.
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Cui, H.1
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Loss of CpG methylation is strongly correlated with loss of histone H3 lysine 9 methylation at DMR-Lit1 in patients with Beckwith-Wiedemann syndrome
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Higashimoto K., Urano T., Sugiura K., Yatsuki H., Joh K., Zhao W., Iwakawa M., Oha H., Osimura M., Niikawa N.et al. Loss of CpG methylation is strongly correlated with loss of histone H3 lysine 9 methylation at DMR-Lit1 in patients with Beckwith-Wiedemann syndrome. Am J Hum Genet. 73:2003;948-956.
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Mann M.R., Chung Y.G., Nolen L.D., Verona R.I., Latham K.E., Bartolomei M.S. Disruption of imprinted gene methylation and expression in cloned preimplantation stage mouse embryos. Biol Reprod. 69:2003;902-914.
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Intracytoplasmic sperm injection may increase the risk of imprinting defects
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Cox G.F., Burger J., Lip V., Mau U.A., Sperling K., Wu B.L., Horsthemke B. Intracytoplasmic sperm injection may increase the risk of imprinting defects. Am J Hum Genet. 71:2002;162-164.
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DeBaun M.R., Niemitz E.L., Feinberg A.P. Association of in vitro fertilization with Beckwith-Wiedemann syndrome and epigenetic alterations of LIT1 and H19. Am J Hum Genet. 72:2003;156-160.
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0038663165
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Folate treatment and unbalanced methylation and changes of allelic expression induced by hyperhomocysteinaemia in patients with uranemia
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Hyper-homocysteinaemia is a genetic disorder in which levels of S-adenosyl-homocysteine are moderately increased. The latter is an inhibitor of S-adenosylmethionine-dependent methyltransferases. In patients, imprinted genes were found to have strongly reduced levels of DNA methylation and were expressed from both the parental alleles. Folate treatment, a commonly used therapy for this disease, restored methylation levels to normal and corrected the allelic patterns of gene expression. This work illustrates how the diet can influence the somatic maintenance of imprinting.
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Ingrosso D., Cimmino A., Perna A.F., Masella L., De Santo N.G., De Bonis M.L., Vacca M., D'Esposito M., D'Urso M., Galetti P.et al. Folate treatment and unbalanced methylation and changes of allelic expression induced by hyperhomocysteinaemia in patients with uranemia. Lancet. 361:2003;1693-1699 Hyper-homocysteinaemia is a genetic disorder in which levels of S-adenosyl-homocysteine are moderately increased. The latter is an inhibitor of S-adenosylmethionine-dependent methyltransferases. In patients, imprinted genes were found to have strongly reduced levels of DNA methylation and were expressed from both the parental alleles. Folate treatment, a commonly used therapy for this disease, restored methylation levels to normal and corrected the allelic patterns of gene expression. This work illustrates how the diet can influence the somatic maintenance of imprinting.
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Lancet
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Ingrosso, D.1
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