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Epigenetic Mechanisms of Genomic Imprinting: Common Themes in the Regulation of Imprinted Regions in Mammals, Plants, and Insects

DOI: 10.1155/2012/585024

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Abstract:

Genomic imprinting is a form of epigenetic inheritance whereby the regulation of a gene or chromosomal region is dependent on the sex of the transmitting parent. During gametogenesis, imprinted regions of DNA are differentially marked in accordance to the sex of the parent, resulting in parent-specific expression. While mice are the primary research model used to study genomic imprinting, imprinted regions have been described in a broad variety of organisms, including other mammals, plants, and insects. Each of these organisms employs multiple, interrelated, epigenetic mechanisms to maintain parent-specific expression. While imprinted genes and imprint control regions are often species and locus-specific, the same suites of epigenetic mechanisms are often used to achieve imprinted expression. This review examines some examples of the epigenetic mechanisms responsible for genomic imprinting in mammals, plants, and insects. 1. Introduction Epigenetic regulation of the genome is a critical facet of development. Epigenetic control of gene expression allows heritable changes in gene expression without the need for alterations in DNA sequence. This is achieved through the recruitment of molecular processes that assist transcription, block transcription, or degrade existing transcripts. Genomic imprinting is an epigenetic process that marks DNA in a sex-dependent manner, resulting in the differential expression of a gene depending on its parent of origin. Achieving an imprint requires establishing meiotically stable male and female imprints during gametogenesis and maintaining the imprinted state through DNA replication in the somatic cells of the embryo. Erasure of the preceding generation’s imprint occurs in the germ line, followed by imprint reestablishment, in accordance with the sex of the organism. Each step in this imprinting process requires epigenetic marks to be interpreted by the genome and acted upon accordingly to result in parent-specific gene expression. Genomic imprinting has been widely reported in eutherian mammals and marsupials [1–3]. Mice comprise the primary research model organism for the study of genomic imprinting. Approximately one hundred imprinted genes have been identified in mice with many more predicted to be present [2, 4]. This review considers imprinting to include chromosomal domains that direct imprinted epigenetic regulation, even if endogenous transcriptional units have yet to be identified as imprinting targets. Many imprinted genes in mice are developmentally important, linked to the formation of the placenta, or

References

[1]  W. Reik and J. Walter, “Genomic imprinting: parental influence on the genome,” Nature Reviews Genetics, vol. 2, no. 1, pp. 21–32, 2001.
[2]  I. M. Morison, J. P. Ramsay, and H. G. Spencer, “A census of mammalian imprinting,” Trends in Genetics, vol. 21, no. 8, pp. 457–465, 2005.
[3]  M. B. Renfree, T. A. Hore, G. Shaw, J. A. Marshall Graves, and A. J. Pask, “Evolution of genomic imprinting: insights from marsupials and monotremes,” Annual Review of Genomics and Human Genetics, vol. 10, pp. 241–262, 2009.
[4]  C. M. Brideau, K. E. Eilertson, J. A. Hagarman, C. D. Bustamante, and P. D. Soloway, “Successful computational prediction of novel imprinted genes from epigenomic features,” Molecular and Cellular Biology, vol. 30, no. 13, pp. 3357–3370, 2010.
[5]  B. Tycko and I. M. Morison, “Physiological functions of imprinted genes,” Journal of Cellular Physiology, vol. 192, no. 3, pp. 245–258, 2002.
[6]  K. Delaval and R. Feil, “Epigenetic regulation of mammalian genomic imprinting,” Current Opinion in Genetics and Development, vol. 14, no. 2, pp. 188–195, 2004.
[7]  H. Royo and J. Cavaillé, “Non-coding RNAs in imprinted gene clusters,” Biology of the Cell, vol. 100, no. 3, pp. 149–166, 2008.
[8]  D. Monk, P. Arnaud, S. Apostolidou et al., “Limited evolutionary conservation of imprinting in the human placenta,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 17, pp. 6623–6628, 2006.
[9]  O. Garnier, S. Laoueillé-Duprat, and C. Spillane, “Genomic imprinting in plants,” Epigenetics, vol. 3, no. 1, pp. 14–20, 2008.
[10]  M. T. Raissig, C. Baroux, and U. Grossniklaus, “Regulation and flexibility of genomic imprinting during seed development,” Plant Cell, vol. 23, no. 1, pp. 16–26, 2011.
[11]  V. Lloyd, “Parental imprinting in Drosophila,” Genetica, vol. 109, no. 1-2, pp. 35–44, 2000.
[12]  R. A. McGowan and C. C. Martin, “DNA methylation and genome imprinting in the zebrafish, Danio rerio: some evolutionary ramifications,” Current Opinion in Genetics & Development, vol. 75, no. 5, pp. 499–506, 1997.
[13]  C. J. Bean, C. E. Schaner, and W. G. Kelly, “Meiotic pairing and imprinted X chromatin assembly in Caenorhabditis elegans,” Nature Genetics, vol. 36, no. 1, pp. 100–105, 2004.
[14]  K. Sha and A. Fire, “Imprinting capacity of gamete lineages in Caenorhabditis elegans,” Genetics, vol. 170, no. 4, pp. 1633–1652, 2005.
[15]  S. Suzuki, R. Ono, T. Narita et al., “Retrotransposon silencing by DNA methylation can drive mammalian genomic imprinting,” PLoS Genetics, vol. 3, no. 4, p. e55, 2007.
[16]  A. J. Pask, A. T. Papenfuss, E. I. Ager, K. A. McColl, T. P. Speed, and M. B. Renfree, “Analysis of the platypus genome suggests a transposon origin for mammalian imprinting,” Genome Biology, vol. 10, no. 1, p. R1, 2009.
[17]  F. Pardo-Manuel de Villena, E. De la Casa-Esperón, and C. Sapienza, “Natural selection and the function of genome imprinting: beyond the silenced minority,” Trends in Genetics, vol. 16, no. 12, pp. 573–579, 2000.
[18]  C. Sapienza, A. C. Peterson, J. Rossant, and R. Balling, “Degree of methylation of transgenes is dependent on gamete of origin,” Nature, vol. 328, no. 6127, pp. 251–254, 1987.
[19]  W. Reik, A. Collick, and M. L. Norris, “Genomic imprinting determines methylation of parental alleles in transgenic mice,” Nature, vol. 328, no. 6127, pp. 248–251, 1987.
[20]  F. Spada, A. Haemmer, D. Kuch et al., “DNMT1 but not its interaction with the replication machinery is required for maintenance of DNA methylation in human cells,” Journal of Cell Biology, vol. 176, no. 5, pp. 565–571, 2007.
[21]  W. Xiao, R. D. Custard, R. C. Brown et al., “DNA methylation is critical for Arabidopsis embroyogenesis and seed viability,” Plant Cell, vol. 18, no. 4, pp. 805–814, 2006.
[22]  F. Lyko, B. H. Ramsahoye, and R. Jaenisch, “DNA methylation in Drosophila melanogaster,” Nature, vol. 408, no. 6812, pp. 538–540, 2000.
[23]  S. L. Berger, “Histone modifications in transcriptional regulation,” Current Opinion in Genetics and Development, vol. 12, no. 2, pp. 142–148, 2002.
[24]  P. Cheung and P. Lau, “Epigenetic regulation by histone methylation and histone variants,” Molecular Endocrinology, vol. 19, no. 3, pp. 563–573, 2005.
[25]  M. Tariq and J. Paszkowski, “DNA and histone methylation in plants,” Trends in Genetics, vol. 20, no. 6, pp. 244–251, 2004.
[26]  H. Cedar and Y. Bergman, “Linking DNA methylation and histone modification: patterns and paradigms,” Nature Reviews Genetics, vol. 10, no. 5, pp. 295–304, 2009.
[27]  R. T. Kamakaka, “Heterochromatin: proteins in flux lead to stable repression,” Current Biology, vol. 13, no. 8, pp. R317–R319, 2003.
[28]  J. C. Eissenberg and S. C. Elgin, “The HP1 protein family: getting a grip on chromatin,” Current Opinion in Genetics and Development, vol. 10, no. 2, pp. 204–210, 2000.
[29]  S. I. S. Grewal and S. C. R. Elgin, “Heterochromatin: new possibilities for the inheritance of structure,” Current Opinion in Genetics and Development, vol. 12, no. 2, pp. 178–187, 2002.
[30]  T. C. James and S. C. Elgin, “Identification of a nonhistone chromosomal protein associated with heterochromatin in Drosophila melanogaster and its gene,” Molecular and Cellular Biology, vol. 6, no. 11, pp. 3862–3872, 1986.
[31]  V. Orlando, “Polycomb, epigenomes, and control of cell identity,” Cell, vol. 112, no. 5, pp. 599–606, 2003.
[32]  W. Filipowicz, “RNAi: the nuts and bolts of the RISC machine,” Cell, vol. 122, no. 1, pp. 17–20, 2005.
[33]  G. Tang, “siRNA and miRNA: an insight into RISCs,” Trends in Biochemical Sciences, vol. 30, no. 2, pp. 106–114, 2005.
[34]  Y. Zhang and L. Qu, “Non-coding RNAs and the acquisition of genomic imprinting in mammals,” Science in China C, vol. 52, no. 3, pp. 195–204, 2009.
[35]  I. Djupedal and K. Ekwall, “Epigenetics: heterochromatin meets RNAi,” Cell Research, vol. 19, no. 3, pp. 282–295, 2009.
[36]  B. Hutter, V. Helms, and M. Paulsen, “Tandem repeats in the CpG islands of imprinted genes,” Genomics, vol. 88, no. 3, pp. 323–332, 2006.
[37]  T. Babak, B. DeVeale, C. Armour et al., “Global survey of genomic imprinting by transcriptome sequencing,” Current Biology, vol. 18, no. 22, pp. 1735–1741, 2008.
[38]  M. S. Bartolomei, S. Zemel, and S. M. Tilghman, “Parental imprinting of the mouse H19 gene,” Nature, vol. 351, no. 6322, pp. 153–155, 1991.
[39]  T. M. DeChiara, E. J. Robertson, and A. Efstratiadis, “Parental imprinting of the mouse insulin-like growth factor II gene,” Cell, vol. 64, no. 4, pp. 849–859, 1991.
[40]  N. Giannoukakis, C. Deal, J. Paquette, C. G. Goodyer, and C. Polychronakos, “Parental genomic imprinting of the human IGF2 gene,” Nature Genetics, vol. 4, no. 1, pp. 98–101, 1993.
[41]  Y. Zhang and B. Tycko, “Monoallelic expression of the human H19 gene,” Nature Genetics, vol. 1, no. 1, pp. 40–44, 1992.
[42]  S. V. Dindot, K. C. Kent, B. Evers, N. Loskutoff, J. Womack, and J. A. Piedrahita, “Conservation of genomic imprinting at the XIST, IGF2, and GTL2 loci in the bovine,” Mammalian Genome, vol. 15, no. 12, pp. 966–974, 2004.
[43]  B. R. Lawton, L. Sevigny, C. Obergfell, D. Reznick, R. J. O'Neill, and M. J. O'Neill, “Allelic expression of IGF2 in live-bearing, matrotrophic fishes,” Development Genes and Evolution, vol. 215, no. 4, pp. 207–212, 2005.
[44]  C. M. Nolan, J. Keith Killian, J. N. Petitte, and R. L. Jirtle, “Imprint status of M6P/IGF2R and IGF2 in chickens,” Development Genes and Evolution, vol. 211, no. 4, pp. 179–183, 2001.
[45]  S. Suzuki, M. B. Renfree, A. J. Pask et al., “Genomic imprinting of IGF2, p57KIP2 and PEG1/MEST in a marsupial, the tammar wallaby,” Mechanisms of Development, vol. 122, no. 2, pp. 213–222, 2005.
[46]  A. Thurston, J. Taylor, J. Gardner, K. D. Sinclair, and L. E. Young, “Monoallelic expression of nine imprinted genes in the sheep embryo occurs after the blastocyst stage,” Reproduction, vol. 135, no. 1, pp. 29–40, 2008.
[47]  M. Constancia, W. Dean, S. Lopes, T. Moore, G. Kelsey, and W. Reik, “Deletion of a silencer element in Igf2 results in loss of imprinting independent of H19,” Nature Genetics, vol. 26, no. 2, pp. 203–206, 2000.
[48]  A. Murrell, S. Heeson, L. Bowden et al., “An intragenic methylated region in the imprinted Igf2 gene augments transcription,” EMBO Reports, vol. 2, no. 12, pp. 1101–1106, 2001.
[49]  M. S. Bartolomei, A. L. Webber, M. E. Brunkow, and S. M. Tilghman, “Epigenetic mechanisms underlying the imprinting of the mouse H19 gene,” Genes and Development, vol. 7, no. 9, pp. 1663–1673, 1993.
[50]  K. L. Arney, “H19 and Igf2- Enhancing the confusion?” Trends in Genetics, vol. 19, no. 1, pp. 17–23, 2003.
[51]  K. L. Tucker, C. Beard, J. Dausman et al., “Germ-line passage is required for establishment of methylation and expression patterns of imprinted but not of nonimprinted genes,” Genes and Development, vol. 10, no. 8, pp. 1008–1020, 1996.
[52]  I. Suetake, F. Shinozaki, J. Miyagawa, H. Takeshima, and S. Tajima, “DNMT3L stimulates the DNA methylation activity of Dnmt3a and Dnmt3b through a direct interaction,” Journal of Biological Chemistry, vol. 279, no. 26, pp. 27816–27823, 2004.
[53]  M. Kaneda, M. Okano, K. Hata et al., “Essential role for de novo DNA methyltransferase Dnmt3a in paternal and maternal imprinting,” Nature, vol. 429, no. 6994, pp. 900–903, 2004.
[54]  R. Hirasawa, H. Chiba, M. Kaneda et al., “Maternal and zygotic Dnmt1 are necessary and sufficient for the maintenance of DNA methylation imprints during preimplantation development,” Genes and Development, vol. 22, no. 12, pp. 1607–1616, 2008.
[55]  W. Reik, W. Dean, and J. Walter, “Epigenetic reprogramming in mammalian development,” Science, vol. 293, no. 5532, pp. 1089–1093, 2001.
[56]  N. Lane, W. Dean, S. Erhardt et al., “Resistance of IAPs to methylation reprogramming may provide a mechanism for epigenetic inheritance in the mouse,” Genesis, vol. 35, no. 2, pp. 88–93, 2003.
[57]  M. S. Bartolomei, “Genomic imprinting: employing and avoiding epigenetic processes,” Genes and Development, vol. 23, no. 18, pp. 2124–2133, 2009.
[58]  N. Beaujean, G. Hartshorne, J. Cavilla et al., “Non-conservation of mammalian preimplantation methylation dynamics,” Current Biology, vol. 14, no. 7, pp. R266–R267, 2004.
[59]  J. Hou, L. Liu, J. Zhang et al., “Epigenetic modification of histone 3 at lysine 9 in sheep zygotes and its relationship with DNA methylation,” BMC Developmental Biology, vol. 8, no. 1, article 60, 2008.
[60]  A. Colosimo, G. Di Rocco, V. Curini et al., “Characterization of the methylation status of five imprinted genes in sheep gametes,” Animal Genetics, vol. 40, no. 6, pp. 900–908, 2009.
[61]  K. Y. Park, E. A. Sellars, A. Grinberg, S. P. Huang, and K. Pfeifer, “The H19 differentially methylated region marks the parental origin of a heterologous locus without gametic DNA methylation,” Molecular and Cellular Biology, vol. 24, no. 9, pp. 3588–3595, 2004.
[62]  C. Gebert, D. Kunkel, A. Grinberg, and K. Pfeifer, “H19 imprinting control region methylation requires an imprinted environment only in the male germ line,” Molecular and Cellular Biology, vol. 30, no. 5, pp. 1108–1115, 2010.
[63]  M. R. W. Mann, S. S. Lee, A. S. Doherty et al., “Selective loss of imprinting in the placenta following preimplantation development in culture,” Development, vol. 131, no. 15, pp. 3727–3735, 2004.
[64]  B. A. Market-Velker, L. Zhang, L. S. Magri, A. C. Bonvissuto, and M. R. W. Mann, “Dual effects of superovulation: loss of maternal and paternal imprinted methylation in a dose-dependent manner,” Human Molecular Genetics, vol. 19, no. 1, Article ID ddp465, pp. 36–51, 2010.
[65]  A. Murrell, S. Heeson, and W. Reik, “Interaction between differentially methylated regions partitions the imprinted genes Igf2 and H19 into parent-specific chromatin loops,” Nature Genetics, vol. 36, no. 8, pp. 889–893, 2004.
[66]  J. Gribnau, K. Hochedlinger, K. Hata, E. Li, and R. Jaenisch, “Asynchronous replication timing of imprinted loci is independent of DNA methylation, but consistent with differential subnuclear localization,” Genes and Development, vol. 17, no. 6, pp. 759–773, 2003.
[67]  F. Cerrato, W. Dean, K. Davies et al., “Paternal imprints can be established on the maternal Igf2-H19 locus without altering replication timing of DNA,” Human Molecular Genetics, vol. 12, no. 23, pp. 3123–3132, 2003.
[68]  P. E. Szabó, S. H. E. Tang, F. J. Silva, W. M. K. Tsark, and J. R. Mann, “Role of CTCF binding sites in the Igf2/H19 imprinting control region,” Molecular and Cellular Biology, vol. 24, no. 11, pp. 4791–4800, 2004.
[69]  A. C. Bell and G. Felsenfeld, “Methylation of a CTCF-dependent boundary controls imprinted expression of the Igf2 gene,” Nature, vol. 405, no. 6785, pp. 482–485, 2000.
[70]  A. T. Hark, C. J. Schoenherr, D. J. Katz, R. S. Ingram, J. M. Levorse, and S. M. Tilghman, “CTCF mediates methylation-sensitive enhancer-blocking activity at the H19/Igf2 locus,” Nature, vol. 405, no. 6785, pp. 486–489, 2000.
[71]  S. Lopes, A. Lewis, P. Hajkova et al., “Epigenetic modifications in an imprinting cluster are controlled by a hierarchy of DMRs suggesting long-range chromatin interactions,” Human Molecular Genetics, vol. 12, no. 3, pp. 295–305, 2003.
[72]  A. M. Fedoriw, P. Stein, P. Svoboda, R. M. Schultz, and M. S. Bartolomei, “Transgenic RNAi Reveals Essential Function for CTCF in H19 Gene Imprinting,” Science, vol. 303, no. 5655, pp. 238–240, 2004.
[73]  J. R. Weidman, S. K. Murphy, C. M. Nolan, F. S. Dietrich, and R. L. Jirtle, “Phylogenetic footprint analysis of IGF2 in extant mammals,” Genome Research, vol. 14, no. 9, pp. 1726–1732, 2004.
[74]  G. N. Filippova, “Genetics and epigenetics of the multifunctional protein CTCF,” Current Topics in Developmental Biology, vol. 80, pp. 337–360, 2008.
[75]  T. Li, J. F. Hu, X. Qiu et al., “CTCF regulates allelic expression of Igf2 by orchestrating a promoter-polycomb repressive complex 2 intrachromosomal loop,” Molecular and Cellular Biology, vol. 28, no. 20, pp. 6473–6482, 2008.
[76]  S. Kurukuti, V. K. Tiwari, G. Tavoosidana et al., “CTCF binding at the H19 imprinting control region mediates maternally inherited higher-order chromatin conformation to restrict enhancer access to Igf2,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 28, pp. 10684–10689, 2006.
[77]  L. B. Wan and M. S. Bartolomei, “Regulation of imprinting in clusters: noncoding RNAs versus insulators,” Advances in Genetics, vol. 61, pp. 207–223, 2008.
[78]  D. P. Barlow, R. Stoger, B. G. Herrmann, K. Saito, and N. Schweifer, “The mouse insulin-like growth factor type-2 receptor is imprinted and closely linked to the Tme locus,” Nature, vol. 349, no. 6304, pp. 84–87, 1991.
[79]  J. F. Wilkins and D. Haig, “What good is genomic imprinting: the function of parent-specific gene expression,” Nature Reviews Genetics, vol. 4, no. 5, pp. 359–368, 2003.
[80]  F. Sleutels, R. Zwart, and D. P. Barlow, “The non-coding Air RNA is required for silencing autosomal imprinted genes,” Nature, vol. 415, no. 6873, pp. 810–813, 2002.
[81]  T. H. Vu, T. Li, and A. R. Hoffman, “Promoter-restricted histone code, not the differentially methylated DNA regions or antisense transcripts, marks the imprinting status of IGF2R in human and mouse,” Human Molecular Genetics, vol. 13, no. 19, pp. 2233–2245, 2004.
[82]  D. N. Ciccone, H. Su, S. Hevi et al., “KDM1B is a histone H3K4 demethylase required to establish maternal genomic imprints,” Nature, vol. 461, no. 7262, pp. 415–418, 2009.
[83]  K. R. McEwen and A. C. Ferguson-Smith, “Distinguishing epigenetic marks of developmental and imprinting regulation,” Epigenetics and Chromatin, vol. 3, no. 1, article 2, 2010.
[84]  P. Singh, X. Wu, D. -H. Lee et al., “Chromosome-wide analysis of parental allele-specific chromatin and DNA methylation,” Molecular and Cellular Biology, vol. 31, no. 8, pp. 1757–1770, 2011.
[85]  A. M. Lindroth, J. P. Yoon, C. M. McLean et al., “Antagonism between DNA and H3K27 methylation at the imprinted Rasgrf1 locus,” PLoS Genetics, vol. 4, no. 8, Article ID e1000145, 2008.
[86]  A. Wutz, O. W. Smrzka, N. Schweifer, K. Schellander, E. F. Wagner, and D. P. Barlow, “Imprinted expression of the Igf2r gene depends on an intronic CpG island,” Nature, vol. 389, no. 6652, pp. 745–749, 1997.
[87]  F. Sleutels, G. Tjon, T. Ludwig, and D. P. Barlow, “Imprinted silencing of Slc22a2 and Slc22a3 does not need transcriptional overlap between Igf2r and Air,” EMBO Journal, vol. 22, no. 14, pp. 3696–3704, 2003.
[88]  T. Nagano, J. A. Mitchell, L. A. Sanz et al., “The Air noncoding RNA epigenetically silences transcription by targeting G9a to chromatin,” Science, vol. 322, no. 5908, pp. 1717–1720, 2008.
[89]  C. I. M. Seidl, S. H. Stricker, and D. P. Barlow, “The imprinted Air ncRNA is an atypical RNAPII transcript that evades splicing and escapes nuclear export,” EMBO Journal, vol. 25, no. 15, pp. 3565–3575, 2006.
[90]  S. H. Stricker, L. Steenpass, F. M. Pauler et al., “Silencing and transcriptional properties of the imprinted Airn ncRNA are independent of the endogenous promoter,” EMBO Journal, vol. 27, no. 23, pp. 3116–3128, 2008.
[91]  M. C. Golding, L. S. Magri, L. Zhang, S. A. Lalone, M. J. Higgins, and M. R.W. Mann, “Depletion of kcnq1ot1 non-coding rna does not affect imprinting maintenance in stem cells,” Development, vol. 138, no. 17, pp. 3667–3678, 2011.
[92]  Y. Zeng, R. Yi, and B. R. Cullen, “MicroRNAs and small interfering RNAs can inhibit mRNA expression by similar mechanisms,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 17, pp. 9779–9784, 2003.
[93]  C. Charlier, K. Segers, D. Wagenaar et al., “Human-ovine comparative sequencing of a 250-kb imprinted domain encompassing the callipyge (clpg) locus and identification of six imprinted transcripts: DLK1, DAT, GTL2, PEG11, antiPEG11, and MEG8,” Genome Research, vol. 11, no. 5, pp. 850–862, 2001.
[94]  H. Seitz, N. Youngson, S. P. Lin et al., “Imprinted microRNA genes transcribed antisense to a reciprocally imprinted retrotransposon-like gene,” Nature Genetics, vol. 34, no. 3, pp. 261–262, 2003.
[95]  S. P. Lin, N. Youngson, S. Takada et al., “Asymmetric regulation of imprinting on the maternal and paternal chromosomes at the Dlk1-Gtl2 imprinted cluster on mouse chromosome 12,” Nature Genetics, vol. 35, no. 1, pp. 97–102, 2003.
[96]  K. Byrne, M. L. Colgrave, T. Vuocolo et al., “The imprinted retrotransposon-like gene PEG11 (RTL1) is expressed as a full-length protein in skeletal muscle from Callipyge sheep,” PLoS ONE, vol. 5, no. 1, Article ID e8638, 2010.
[97]  E. Davis, F. Caiment, X. Tordoir et al., “RNAi-mediated allelic trans-interaction at the imprinted Rtl1/Peg11 locus,” Current Biology, vol. 15, no. 8, pp. 743–749, 2005.
[98]  K. E. Latham, “X chromosome imprinting and inactivation in preimplantation mammalian embryos,” Trends in Genetics, vol. 21, no. 2, pp. 120–127, 2005.
[99]  A. A. Andersen and B. Panning, “Epigenetic gene regulation by noncoding RNAs,” Current Opinion in Cell Biology, vol. 15, no. 3, pp. 281–289, 2003.
[100]  S. Kalantry, S. Purushothaman, R. B. Bowen, J. Starmer, and T. Magnuson, “Evidence of Xist RNA-independent initiation of mouse imprinted X-chromosome inactivation,” Nature, vol. 460, no. 7255, pp. 647–651, 2009.
[101]  Y. Ogawa, B. K. Sun, and J. T. Lee, “Intersection of the RNA interference and X-inactivation pathways,” Science, vol. 320, no. 5881, pp. 1336–1341, 2008.
[102]  J. L. Kermicle, “Dependenct of the R-Mottled aleurone phenotype in maize on mode of sexual transmission,” Genetics, vol. 66, no. 1, pp. 69–85, 1970.
[103]  T. Kinoshita, A. Miura, Y. Choi et al., “One-way control of FWA imprinting in Arabidopsis endosperm by DNA methylation,” Science, vol. 303, no. 5657, pp. 521–523, 2004.
[104]  M. Gehring, J. H. Huh, T. F. Hsieh et al., “DEMETER DNA glycosylase establishes MEDEA polycomb gene self-imprinting by allele-specific demethylation,” Cell, vol. 124, no. 3, pp. 495–506, 2006.
[105]  Y. Choi, M. Gehring, L. Johnson et al., “DEMETER, a DNA glycosylase domain protein, is required for endosperm gene imprinting and seed viability in Arabidopsis,” Cell, vol. 110, no. 1, pp. 33–42, 2002.
[106]  P. E. Jullien, T. Kinoshita, N. Ohad, and F. Berger, “Maintenance of DNA methylation during the Arabidopsis life cycle is essential for parental imprinting,” Plant Cell, vol. 18, no. 6, pp. 1360–1372, 2006.
[107]  Z. Lippman and R. Martienssen, “The role of RNA interference in heterochromatic silencing,” Nature, vol. 431, no. 7006, pp. 364–370, 2004.
[108]  M. B. Wang, S. V. Wesley, E. J. Finnegan, N. A. Smith, and P. M. Waterhouse, “Replicating satellite RNA induces sequence-specific DNA methylation and truncated transcripts in plants,” RNA, vol. 7, no. 1, pp. 16–28, 2001.
[109]  Z. Lippman, B. May, C. Yordan, T. Singer, and R. Martienssen, “Distinct mechanisms determine transposon inheritance and methylation via small interfering RNA and histone modification,” PLoS Biology, vol. 1, no. 3, p. E67, 2003.
[110]  S. W. L. Chan, D. Zilberman, Z. Xie, L. K. Johansen, J. C. Carrington, and S. E. Jacobsen, “RNA silencing genes control de novo DNA methylation,” Science, vol. 303, no. 5662, p. 1336, 2004.
[111]  W. Xiao, M. Gehring, Y. Choi et al., “Imprinting of the MEA polycomb gene is controlled by antagonism between MET1 methyltransferase and DME glycosylase,” Developmental Cell, vol. 5, no. 6, pp. 891–901, 2003.
[112]  M. Luo, P. Bilodeau, E. S. Dennis, W. J. Peacock, and A. Chaudhury, “Expression and parent-of-origin effects for FIS2, MEA, and FIE in the endosperm and embryo of developing Arabidopsis seeds,” Proceedings of the National Academy of Sciences of the United States of America, vol. 97, no. 19, pp. 10637–10642, 2000.
[113]  P. E. Jullien, A. Katz, M. Oliva, N. Ohad, and F. Berger, “Polycomb group complexes self-regulate imprinting of the polycomb group gene MEDEA in Arabidopsis,” Current Biology, vol. 16, no. 5, pp. 486–492, 2006.
[114]  C. K?hler, D. R. Page, V. Gagliardini, and U. Grossniklaus, “The Arabidopsis thaliana MEDEA Polycomb group protein controls expression of PHERES1 by parental imprinting,” Nature Genetics, vol. 37, no. 1, pp. 28–30, 2005.
[115]  C. K?hler, L. Hennig, C. Spillane, S. Pien, W. Gruissem, and U. Grossniklaus, “The Polycomb-group protein MEDEA regulates seed development by controlling expression of the MADS-box gene PHERES1,” Genes and Development, vol. 17, no. 12, pp. 1540–1553, 2003.
[116]  X. Wang, P. D. Soloway, and A. G. Clark, “A survey for novel imprinted genes in the mouse placenta by mRNA-seq,” Genetics, vol. 189, no. 1, pp. 109–122, 2011.
[117]  S. Jahnke and S. Scholten, “Epigenetic resetting of a gene imprinted in plant embryos,” Current Biology, vol. 19, no. 19, pp. 1677–1681, 2009.
[118]  C. W. Metz, “Chromosomes and sex in Sciara,” Science, vol. 61, no. 1573, pp. 212–214, 1925.
[119]  F. Schrader, “The chromosomes of Pseudococcus nipae,” Biological Bulletin, vol. 40, no. 5, pp. 259–270, 1921.
[120]  H. V. Crouse, “The controlling element in sex chromosome behavior in Sciara,” Genetics, vol. 45, no. 10, pp. 1429–1443, 1960.
[121]  B. B. Normark, “The evolution of alternative genetic systems in insects,” Annual Review of Entomology, vol. 48, pp. 397–423, 2003.
[122]  M. Anaka, A. Lynn, P. McGinn, and V. K. Lloyd, “Genomic imprinting in Drosophila has properties of both mammalian and insect imprinting,” Development Genes and Evolution, vol. 219, no. 2, pp. 59–66, 2009.
[123]  K. A. Maggert and K. G. Golic, “The Y chromosome of Drosophila melanogaster exhibits chromosome-wide imprinting,” Genetics, vol. 162, no. 3, pp. 1245–1258, 2002.
[124]  B. S. Haller and R. C. Woodruff, “Varied expression of a Y-linked P[W+] insert due to imprinting in Drosophila melanogaster,” Genome, vol. 43, no. 2, pp. 285–292, 2000.
[125]  J. Cohen, “Position-effect variegation at several closely linked loci in Drosophila melanogaster,” Gerontologia Clinica, vol. 47, pp. 647–659, 1962.
[126]  V. K. Lloyd, D. A. Sinclair, and T. A. Grigliatti, “Genomic imprinting and position-effect variegation in Drosophila melanogaster,” Genetics, vol. 151, no. 4, pp. 1503–1516, 1999.
[127]  R. W. Hardy, D. L. Lindsley, and K. J. Livak, “Cytogenetic analysis of a segment of the Y chromosome of Drosophila melanogaster,” Genetics, vol. 107, no. 4, pp. 591–610, 1984.
[128]  V. Joanis and V. Lloyd, “Genomic imprinting in Drosophila is maintained by the products of Suppressor of variegation and trithorax group, but not Polycomb group, genes,” Molecular Genetics and Genomics, vol. 268, no. 1, pp. 103–112, 2002.
[129]  T. Rudolph, M. Yonezawa, S. Lein et al., “Heterochromatin formation in Drosophila is initiated through active removal of H3K4 Methylation by the LSD1 Homolog SU(VAR)3-3,” Molecular Cell, vol. 26, no. 1, pp. 103–115, 2007.
[130]  S. Takeda and J. Paszkowski, “DNA methylation and epigenetic inheritance during plant gametogenesis,” Chromosoma, vol. 115, no. 1, pp. 27–35, 2005.
[131]  J. E. Phillips and V. G. Corces, “CTCF: master weaver of the genome,” Cell, vol. 137, no. 7, pp. 1194–1211, 2009.
[132]  T. A. Schoborg and M. Labrador, “The phylogenetic distribution of non-CTCF insulator proteins is limited to insects and reveals that beaf-32 is drosophila lineage specific,” Journal of Molecular Evolution, vol. 70, no. 1, pp. 74–84, 2010.
[133]  W. A. MacDonald, D. Menon, N. J. Bartlett et al., “The Drosophila homolog of the mammalian imprint regulator, CTCF, maintains the maternal genomic imprint in Drosophila melanogaster,” BMC Biology, vol. 8, no. 1, article105, 2010.
[134]  V. K. Lloyd, Unpublished Observations, Mount Allison University, Sackville NB, Canada, 2011.
[135]  T. I. Gerasimova and V. G. Corces, “Polycomb and trithorax group proteins mediate the function of a chromatin insulator,” Cell, vol. 92, no. 4, pp. 511–521, 1998.
[136]  C. J. Schoenherr, J. M. Levorse, and S. M. Tilghman, “CTCF maintains differential methylation at the Igf2/H19 locus,” Nature Genetics, vol. 33, no. 1, pp. 66–69, 2003.
[137]  A. J. Haigh and V. K. Lloyd, “Loss of genomic imprinting in Drosophila clones,” Genome, vol. 49, no. 8, pp. 1043–1046, 2006.
[138]  J. M. Greally, T. A. Gray, J. M. Gabriel, L. Q. Song, S. Zemel, and R. D. Nicholls, “Conserved characteristics of heterochromatin-forming DNA at the 15q11-q13 imprinting center,” Proceedings of the National Academy of Sciences of the United States of America, vol. 96, no. 25, pp. 14430–14435, 1999.
[139]  X. Deng and V. H. Meller, “Non-coding RNA in fly dosage compensation,” Trends in Biochemical Sciences, vol. 31, no. 9, pp. 526–532, 2006.
[140]  X. Deng and V. H. Meller, “roX RNAs are required for increased expression of X-linked genes in Drosophila melanogaster males,” Genetics, vol. 174, no. 4, pp. 1859–1866, 2006.
[141]  R. L. Kelley, O. K. Lee, and Y. K. Shim, “Transcription rate of noncoding roX1 RNA controls local spreading of the Drosophila MSL chromatin remodeling complex,” Mechanisms of Development, vol. 125, no. 11-12, pp. 1009–1019, 2008.
[142]  D. U. Menon and V. H. Meller, “Imprinting of the Y chromosome influences dosage compensation in roX1 roX2 Drosophila melanogaster,” Genetics, vol. 183, no. 3, pp. 811–820, 2009.
[143]  P. B. Vrana, J. A. Fossella, P. Matteson, T. Del Rio, M. J. O'Neill, and S. M. Tilghman, “Genetic and epigenetic incompatibilities underlie hybrid dysgenesis in peromyscus,” Nature Genetics, vol. 25, no. 1, pp. 120–124, 2000.
[144]  C. Josefsson, B. Dilkes, and L. Comai, “Parent-dependent loss of gene silencing during interspecies hybridization,” Current Biology, vol. 16, no. 13, pp. 1322–1328, 2006.
[145]  S. Bongiorni, O. Cintio, and G. Prantera, “The relationship between DNA methylation and chromosome imprinting in the Coccid Planococcus citri,” Genetics, vol. 151, no. 4, pp. 1471–1478, 1999.
[146]  S. Bongiorni, M. Pugnali, S. Volpi, D. Bizzaro, P. B. Singh, and G. Prantera, “Epigenetic marks for chromosome imprinting during spermatogenesis in Coccids,” Chromosoma, vol. 118, no. 4, pp. 501–512, 2009.
[147]  S. Bongiorni, B. Pasqualini, M. Taranta, P. B. Singh, and G. Prantera, “Epigenetic regulation of facultative heterochromatinisation in Planococcus citri via the Me(3)K9H3-HP1-Me(3)K20H4 pathway,” Journal of Cell Science, vol. 120, no. 6, pp. 1072–1080, 2007.
[148]  N. Kunert, J. Marhold, J. Stanke, D. Stach, and F. Lyko, “A Dnmt2-like protein mediates DNA methylation in Drosophila,” Development, vol. 130, no. 21, pp. 5083–5090, 2003.
[149]  M. Schaefer, J. P. Steringer, and F. Lyko, “The Drosophila cytosine-5 methyltransferase Dnmt2 is associated with the nuclear matrix and can access DNA during mitosis,” PLoS ONE, vol. 3, no. 1, Article ID e1414, 2008.
[150]  M. J. Lin, L. Y. Tang, M. N. Reddy, and C. K. J. Shen, “DNA methyltransferase gene dDnmt2 and longevity of Drosophila,” Journal of Biological Chemistry, vol. 280, no. 2, pp. 861–864, 2005.
[151]  S. Phalke, O. Nickel, D. Walluscheck, F. Hortig, M. C. Onorati, and G. Reuter, “Retrotransposon silencing and telomere integrity in somatic cells of Drosophila depends on the cytosine-5 methyltransferase DNMT2,” Nature Genetics, vol. 41, no. 6, pp. 696–702, 2009.
[152]  F. Lyko, B. H. Ramsahoye, H. Kashevsky et al., “Mammalian (cytosine-5) methyltransferases cause genomic DNA methylation and lethality in Drosophila,” Nature Genetics, vol. 23, no. 3, pp. 363–366, 1999.
[153]  A. Weyrich, X. Tang, G. Xu, A. Schrattenholz, C. Hunzinger, and W. Hennig, “Mammalian DNMTs in the male germ line DNA of Drosophila,” Biochemistry and Cell Biology, vol. 86, no. 5, pp. 380–385, 2008.
[154]  V. Krauss and G. Reuter, “DNA Methylation in drosophila-a critical evaluation,” Progress in Molecular Biology and Translational Science, vol. 101, pp. 177–191, 2011.
[155]  M. Schaefer and F. Lyko, “Lack of evidence for DNA methylation of Invader4 retroelements in Drosophila and implications for Dnmt2-mediated epigenetic regulation,” Nature Genetics, vol. 42, no. 11, pp. 920–921, 2010.
[156]  F. Lyko, J. D. Brenton, M. A. Surani, and R. Paro, “An imprinting element from the mouse H19 locus functions as a silencer in Drosophila,” Nature Genetics, vol. 16, no. 2, pp. 171–173, 1997.
[157]  F. Lyko, K. Buiting, B. Horsthemke, and R. Paro, “Identification of a silencing element in the human 15q11-q13 imprinting center by using transgenic Drosophila,” Proceedings of the National Academy of Sciences of the United States of America, vol. 95, no. 4, pp. 1698–1702, 1998.
[158]  S. Erhardt, F. Lyko, J. F. X. Ainscough, M. A. Surani, and R. Paro, “Polycomb-group proteins are involved in silencing processes caused by a transgenic element from the murine imprinted H19/Igf2 region in Drosophila,” Development Genes and Evolution, vol. 213, no. 7, pp. 336–344, 2003.
[159]  B. K. Jones, J. Levorse, and S. M. Tilghman, “A human H19 transgene exhibits impaired paternal-specific imprint acquisition and maintenance in mice,” Human Molecular Genetics, vol. 11, no. 4, pp. 411–418, 2002.
[160]  S. M. Blaydes, M. Elmore, T. Yang, and C. I. Brannan, “Analysis of murine Snrpn and human SBRPN gene imprinting in transgenic mice,” Mammalian Genome, vol. 10, no. 6, pp. 549–555, 1999.
[161]  J. D. Brenton, R. A. Drewell, S. Viville et al., “A silencer element identified in Drosophila is required for imprinting of H19 reporter transgenes in mice,” Proceedings of the National Academy of Sciences of the United States of America, vol. 96, no. 16, pp. 9242–9247, 1999.
[162]  S. Schoenfelder, G. Smits, P. Fraser, W. Reik, and R. Paro, “Non-coding transcripts in the H19 imprinting control region mediate gene silencing in transgenic Drosophila,” EMBO Reports, vol. 8, no. 11, pp. 1068–1073, 2007.
[163]  R. A. Drewell, J. D. Brenton, J. F. X. Ainscough et al., “Deletion of a silencer element disrupts H19 imprinting independently of a DNA methylation epigenetic switch,” Development, vol. 127, no. 16, pp. 3419–3428, 2000.
[164]  S. Schoenfelder and R. Paro, “Drosophila Su(Hw) regulates an evolutionarily conserved silencer from the mouse H19 imprinting control region,” Cold Spring Harbor Symposia on Quantitative Biology, vol. 69, pp. 47–54, 2004.
[165]  R. R. Roseman, V. Pirrotta, and P. K. Geyer, “The su(Hw) protein insulates expression of the Drosophila melanogaster white gene from chromosomal position-effects,” EMBO Journal, vol. 12, no. 2, pp. 435–442, 1993.
[166]  K. L. Arney, E. Bae, C. Olsen, and R. A. Drewell, “The human and mouse H19 imprinting control regions harbor an evolutionarily conserved silencer element that functions on transgenes in Drosophila,” Development Genes and Evolution, vol. 216, no. 12, pp. 811–819, 2006.
[167]  X. Zhang, O. Clarenz, S. Cokus et al., “Whole-genome analysis of histone H3 lysine 27 trimethylation in Arabidopsis,” PLoS Biology, vol. 5, no. 5, p. e129, 2007.

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