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Jenuwein T. Molecular biology. An RNA-guided pathway for the epigenome. Science. 297:2002;2215-2218.
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Dernburg A.F., Karpen G.H. A chromosome RNAissance. Cell. 111:2002;159-162.
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Dernburg, A.F.1
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Stevenson D.S., Jarvis P. Chromatin silencing: RNA in the driving seat. Curr. Biol. 13:2003;R13-R15.
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Stevenson, D.S.1
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0033588309
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Epigenetic spreading of the Drosophila dosage compensation complex from roX RNA genes into flanking chromatin
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Kelley R.L., Meller V.H., Gordadze P.R., Roman G., Davis R.L., Kuroda M.I. Epigenetic spreading of the Drosophila dosage compensation complex from roX RNA genes into flanking chromatin. Cell. 98:1999;513-522.
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Kelley, R.L.1
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Activation of transcription through histone H4 acetylation by MOF, an acetyltransferase essential for dosage compensation in Drosophila
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Akhtar A., Becker P.B. Activation of transcription through histone H4 acetylation by MOF, an acetyltransferase essential for dosage compensation in Drosophila. Mol. Cell. 5:2000;367-375.
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Akhtar, A.1
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JIL-1, a chromosomal kinase implicated in regulation of chromatin structure, associates with the male specific lethal (MSL) dosage compensation complex
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Jin Y., Wang Y., Johansen J., Johansen K.M. JIL-1, a chromosomal kinase implicated in regulation of chromatin structure, associates with the male specific lethal (MSL) dosage compensation complex. J. Cell Biol. 149:2000;1005-1010.
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Jin, Y.1
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The NTPase/helicase activities of Drosophila maleless, an essential factor in dosage compensation
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Lee C.G., Chang K.A., Kuroda M.I., Hurwitz J. The NTPase/helicase activities of Drosophila maleless, an essential factor in dosage compensation. EMBO J. 16:1997;2671-2681.
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Lee, C.G.1
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0034597001
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Targeting the chromatin-remodeling MSL complex of Drosophila to its sites of action on the X chromosome requires both acetyl transferase and ATPase activities
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Gu W., Wei X., Pannuti A., Lucchesi J.C. Targeting the chromatin-remodeling MSL complex of Drosophila to its sites of action on the X chromosome requires both acetyl transferase and ATPase activities. EMBO J. 19:2000;5202-5211.
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Gu, W.1
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The roX1 and roX2 RNAs are essential components of the compensasome, which mediates dosage compensation in Drosophila
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Franke A., Baker B.S. The roX1 and roX2 RNAs are essential components of the compensasome, which mediates dosage compensation in Drosophila. Mol. Cell. 4:1999;117-122.
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Franke, A.1
Baker, B.S.2
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12
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0036500632
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The roX genes encode redundant male-specific lethal transcripts required for targeting of the MSL complex
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•], flies lacking only the roX2 transcript were examined, whereas the flies examined in [11] were deleted not only for roX2 but also for some flanking essential genes. MSL2 is not enriched on the X chromosome and is relocalized to autosomal regions in males lacking roX RNAs. The residual MSL2 localization appears to be associated with transcriptional up-regulation, suggesting that a partial MSL complex might retain some activity. The requirement for the roX RNAs in dosage compensation may be for proper localization and spreading from the chromatin entry sites.
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•], flies lacking only the roX2 transcript were examined, whereas the flies examined in [11] were deleted not only for roX2 but also for some flanking essential genes. MSL2 is not enriched on the X chromosome and is relocalized to autosomal regions in males lacking roX RNAs. The residual MSL2 localization appears to be associated with transcriptional up-regulation, suggesting that a partial MSL complex might retain some activity. The requirement for the roX RNAs in dosage compensation may be for proper localization and spreading from the chromatin entry sites.
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EMBO J.
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Meller, V.H.1
Rattner, B.P.2
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13
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2242492681
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Extent of chromatin spreading determined by roX RNA recruitment of MSL proteins
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This work demonstrated that the abundance of the components of the male-specific lethal (MSL) complex determines whether the complex spreads in cis from an autosomal roX transgene. When the MSL:roX RNA ratios are high complexes spread in cis. Increasing the concentration of MSL proteins or decreasing the number of roX genes resulted in increased cis spread from an autosomal roX transgene.
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Park Y., Kelley R.L., Oh H., Kuroda M.I., Meller V.H. Extent of chromatin spreading determined by roX RNA recruitment of MSL proteins. Science. 298:2002;1620-1623 This work demonstrated that the abundance of the components of the male-specific lethal (MSL) complex determines whether the complex spreads in cis from an autosomal roX transgene. When the MSL:roX RNA ratios are high complexes spread in cis. Increasing the concentration of MSL proteins or decreasing the number of roX genes resulted in increased cis spread from an autosomal roX transgene.
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Science
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Park, Y.1
Kelley, R.L.2
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Kuroda, M.I.4
Meller, V.H.5
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14
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0035943606
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Recruitment of the male-specific lethal (MSL) dosage compensation complex to an autosomally integrated roX chromatin entry site correlates with an increased expression of an adjacent reporter gene in male Drosophila
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Henry R.A., Tews B., Li X., Scott M.J. Recruitment of the male-specific lethal (MSL) dosage compensation complex to an autosomally integrated roX chromatin entry site correlates with an increased expression of an adjacent reporter gene in male Drosophila. J. Biol. Chem. 276:2001;31953-31958.
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Henry, R.A.1
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0035341311
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Association and spreading of the Drosophila dosage compensation complex from a discrete roX1 chromatin entry site
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Kageyama Y., Mengus G., Gilfillan G., Kennedy H.G., Stuckenholz C., Kelley R.L., Becker P.B., Kuroda M.I. Association and spreading of the Drosophila dosage compensation complex from a discrete roX1 chromatin entry site. EMBO J. 20:2001;2236-2245.
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Kageyama, Y.1
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Kelley, R.L.6
Becker, P.B.7
Kuroda, M.I.8
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16
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The role of chromosomal RNAs in marking the X for dosage compensation
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Kelley R.L., Kuroda M.I. The role of chromosomal RNAs in marking the X for dosage compensation. Curr. Opin. Gen. Dev. 10:2000;555-561.
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Kelley, R.L.1
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A shift from reversible to irreversible X inactivation is triggered during ES cell differentiation
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Wutz A., Jaenisch R. A shift from reversible to irreversible X inactivation is triggered during ES cell differentiation. Mol. Cell. 5:2000;695-705.
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Mol. Cell
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Wutz, A.1
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Conditional deletion of Xist disrupts histone macroH2A localization but not maintenance of X inactivation [Letter]
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Csankovszki G., Panning B., Bates B., Pehrson J.R., Jaenisch R. Conditional deletion of Xist disrupts histone macroH2A localization but not maintenance of X inactivation [Letter]. Nat. Genet. 22:1999;323-324.
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Csankovszki, G.1
Panning, B.2
Bates, B.3
Pehrson, J.R.4
Jaenisch, R.5
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20
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0037173064
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An ectopic human XIST gene can induce chromosome inactivation in post-differentiation human HT-1080 cells
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Employing XIST autosomal transgenes in HT-1080 cells, this study demonstrates for the first time that certain differentiated cells are susceptible to XIST-RNA-mediated gene silencing. It is not known what feature(s) of these differentiated cells enable them to respond to XIST RNA.
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Hall L.L., Byron M., Sakai K., Carrel L., Willard H.F., Lawrence J.B. An ectopic human XIST gene can induce chromosome inactivation in post-differentiation human HT-1080 cells. Proc. Natl. Acad. Sci. USA. 99:2002;8677-8682 Employing XIST autosomal transgenes in HT-1080 cells, this study demonstrates for the first time that certain differentiated cells are susceptible to XIST-RNA-mediated gene silencing. It is not known what feature(s) of these differentiated cells enable them to respond to XIST RNA.
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(2002)
Proc. Natl. Acad. Sci. USA
, vol.99
, pp. 8677-8682
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Hall, L.L.1
Byron, M.2
Sakai, K.3
Carrel, L.4
Willard, H.F.5
Lawrence, J.B.6
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21
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0036479009
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Chromosomal silencing and localization are mediated by different domains of Xist RNA
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This study examined 48 different Xist RNA deletion mutants for silencing and coating activities. The authors found that coating and silencing were mediated by separable Xist RNA domains. One RNA deletion mutant could coat but not silence the X chromosome. Mutational analysis revealed that the silencing domain consists of 7.5 repeated units corresponding to two RNA stem-loops. RNAs containing both the silencing domain and one of several nonoverlapping domains could coat and silence the chromosome. Thus, several redundant domains, including the silencing domain, contribute to the coating function of Xist RNA.
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Wutz A., Rasmussen T.P., Jaenisch R. Chromosomal silencing and localization are mediated by different domains of Xist RNA. Nat. Genet. 30:2002;167-174 This study examined 48 different Xist RNA deletion mutants for silencing and coating activities. The authors found that coating and silencing were mediated by separable Xist RNA domains. One RNA deletion mutant could coat but not silence the X chromosome. Mutational analysis revealed that the silencing domain consists of 7.5 repeated units corresponding to two RNA stem-loops. RNAs containing both the silencing domain and one of several nonoverlapping domains could coat and silence the chromosome. Thus, several redundant domains, including the silencing domain, contribute to the coating function of Xist RNA.
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Nat. Genet.
, vol.30
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Wutz, A.1
Rasmussen, T.P.2
Jaenisch, R.3
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PNA interference mapping demonstrates functional domains in the noncoding RNA Xist
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Beletskii A., Hong Y.K., Pehrson J., Egholm M., Strauss W.M. PNA interference mapping demonstrates functional domains in the noncoding RNA Xist. Proc. Natl. Acad Sci. USA. 98:2001;9215-9220.
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Beletskii, A.1
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Strauss, W.M.5
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23
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0035861875
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Methylation of histone H3 at Lys-9 is an early mark on the X chromosome during X inactivation
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••] identify an enrichment or 'hot spot' of H3-K9 methylation upstream of the Xist promoter in undifferentiated ES cells. They propose that the association of Xist RNA with the hotspot is the initial event in the spread of the inactivation signal.
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••] identify an enrichment or 'hot spot' of H3-K9 methylation upstream of the Xist promoter in undifferentiated ES cells. They propose that the association of Xist RNA with the hotspot is the initial event in the spread of the inactivation signal.
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(2001)
Cell
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Heard, E.1
Rougeulle, C.2
Arnaud, D.3
Avner, P.4
Allis, C.D.5
Spector, D.L.6
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25
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0034934749
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Imprinted X inactivation maintained by a mouse Polycomb group gene
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The authors identified the first protein demonstrated to have a function in X-chromosome inactivation. The authors knocked out Eed and showed that this protein is required for maintenance of the imprinted inactive X chromosome in extra-embryonic tissues of mice.
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Wang J., Mager J., Chen Y., Schneider E., Cross J.C., Nagy A., Magnuson T. Imprinted X inactivation maintained by a mouse Polycomb group gene. Nat. Genet. 28:2001;371-375 The authors identified the first protein demonstrated to have a function in X-chromosome inactivation. The authors knocked out Eed and showed that this protein is required for maintenance of the imprinted inactive X chromosome in extra-embryonic tissues of mice.
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Wang, J.1
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Schneider, E.4
Cross, J.C.5
Nagy, A.6
Magnuson, T.7
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26
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0031842310
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Characterization of interactions between the mammalian Polycomb-group proteins Enx1/EZH2 and EED suggests the existence of different mammalian Polycomb-group protein complexes
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Sewalt R.G., van der Vlag J., Gunster M.J., Hamer K.M., den Blaauwen J.L., Satijn D.P., Hendrix T., van Driel R., Otte A.P. Characterization of interactions between the mammalian Polycomb-group proteins Enx1/EZH2 and EED suggests the existence of different mammalian Polycomb-group protein complexes. Mol. Cell Biol. 18:1998;3586-3595.
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Sewalt, R.G.1
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Den Blaauwen, J.L.5
Satijn, D.P.6
Hendrix, T.7
Van Driel, R.8
Otte, A.P.9
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27
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0031843056
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Interaction of mouse Polycomb-group (Pc-G) proteins Enx1 and Enx2 with Eed: Indication for separate Pc-G complexes
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van Lohuizen M., Tijms M., Voncken J.W., Schumacher A., Magnuson T., Wientjens E. Interaction of mouse Polycomb-group (Pc-G) proteins Enx1 and Enx2 with Eed: indication for separate Pc-G complexes. Mol. Cell Biol. 18:1998;3572-3579.
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Van Lohuizen, M.1
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Voncken, J.W.3
Schumacher, A.4
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Wientjens, E.6
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28
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0037172659
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Mitotically stable association of Polycomb group proteins Eed and Enx1 with the inactive X chromosome in trophoblast stem cells
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The authors use immunofluorescence to demonstrate that Eed and Enx1, which function in maintenance of imprinted X-chromosome inactivation, accumulate on the inactive X chromosome in mouse cells derived from the extra-embryonic lineage.
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Mak W., Baxter J., Silva J., Newall A.E., Otte A.P., Brockdorff N. Mitotically stable association of Polycomb group proteins Eed and Enx1 with the inactive X chromosome in trophoblast stem cells. Curr. Biol. 12:2002;1016-1020 The authors use immunofluorescence to demonstrate that Eed and Enx1, which function in maintenance of imprinted X-chromosome inactivation, accumulate on the inactive X chromosome in mouse cells derived from the extra-embryonic lineage.
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Curr. Biol.
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Mak, W.1
Baxter, J.2
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Brockdorff, N.6
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30
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0036830642
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Role of histone H3 lysine 27 methylation in Polycomb-group silencing
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••]. These observations suggest that H3-K27 methylation may be a functionally important modification on the inactive X chromosome.
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••]. These observations suggest that H3-K27 methylation may be a functionally important modification on the inactive X chromosome.
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(2002)
Science
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Cao, R.1
Wang, L.2
Wang, H.3
Xia, L.4
Erdjument-Bromage, H.5
Tempst, P.6
Jones, R.S.7
Zhang, Y.8
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31
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0036338205
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Histone H3 lysine 9 methylation is an epigenetic imprint of facultative heterochromatin
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This work demonstrates an enrichment for H3-K9 methylation on the inactive X chromosome (Xi) by immunofluorescence. This methylation occurs independently of Suv39h1 and Suv39h2, the histone methyltransferases responsible for methylating H3-K9 at other regions of heterochromatin such as centromeres. This observation suggests that there may be an Xi-specific histone methyltransferase complex.
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Peters A.H., Mermoud J.E., O'Carroll D., Pagani M., Schweizer D., Brockdorff N., Jenuwein T. Histone H3 lysine 9 methylation is an epigenetic imprint of facultative heterochromatin. Nat. Genet. 30:2002;77-80 This work demonstrates an enrichment for H3-K9 methylation on the inactive X chromosome (Xi) by immunofluorescence. This methylation occurs independently of Suv39h1 and Suv39h2, the histone methyltransferases responsible for methylating H3-K9 at other regions of heterochromatin such as centromeres. This observation suggests that there may be an Xi-specific histone methyltransferase complex.
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Nat. Genet.
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Peters, A.H.1
Mermoud, J.E.2
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Pagani, M.4
Schweizer, D.5
Brockdorff, N.6
Jenuwein, T.7
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32
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0037099413
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G9a histone methyltransferase plays a dominant role in euchromatic histone H3 lysine 9 methylation and is essential for early embryogenesis
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Tachibana M., Sugimoto K., Nozaki M., Ueda J., Ohta T., Ohki M., Fukuda M., Takeda N., Niida H., Kato H.et al. G9a histone methyltransferase plays a dominant role in euchromatic histone H3 lysine 9 methylation and is essential for early embryogenesis. Genes Dev. 16:2002;1779-1791.
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Tachibana, M.1
Sugimoto, K.2
Nozaki, M.3
Ueda, J.4
Ohta, T.5
Ohki, M.6
Fukuda, M.7
Takeda, N.8
Niida, H.9
Kato, H.10
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33
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18744372123
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BRCA1 supports XIST RNA concentration on the inactive X chromosome
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The authors demonstrate that BRCA1 is required for XIST RNA coating of the inactive X chromosome (Xi). Depletion of BRCA1 results in a loss of chromosome coating by XIST RNA, which leads to the reactivation of some genes on the Xi, as expected from previous observations that Xist plays a minor role in Xi maintenance, albeit a minor one. BRCA1 co-localizes with the Xi in S phase in multiple female cell lines. BRCA1 is the only protein known to affect Xist RNA coating activity, but it is not known how BRCA1 supports coating of the Xi.
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Ganesan S., Silver D.P., Greenberg R.A., Avni D., Drapkin R., Miron A., Mok S.C., Randrianarison V., Brodie S., Salstrom J.et al. BRCA1 supports XIST RNA concentration on the inactive X chromosome. Cell. 111:2002;393-405 The authors demonstrate that BRCA1 is required for XIST RNA coating of the inactive X chromosome (Xi). Depletion of BRCA1 results in a loss of chromosome coating by XIST RNA, which leads to the reactivation of some genes on the Xi, as expected from previous observations that Xist plays a minor role in Xi maintenance, albeit a minor one. BRCA1 co-localizes with the Xi in S phase in multiple female cell lines. BRCA1 is the only protein known to affect Xist RNA coating activity, but it is not known how BRCA1 supports coating of the Xi.
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Cell
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Ganesan, S.1
Silver, D.P.2
Greenberg, R.A.3
Avni, D.4
Drapkin, R.5
Miron, A.6
Mok, S.C.7
Randrianarison, V.8
Brodie, S.9
Salstrom, J.10
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34
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Lee C.G., Hurwitz J. Human RNA helicase A is homologous to the maleless protein of Drosophila. J. Biol. Chem. 268:1993;16822-16830.
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Lee, C.G.1
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BRCA1 protein is linked to the RNA polymerase II holoenzyme complex via RNA helicase A
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Anderson S.F., Schlegel B.P., Nakajima T., Wolpin E.S., Parvin J.D. BRCA1 protein is linked to the RNA polymerase II holoenzyme complex via RNA helicase A. Nat. Genet. 19:1998;254-256.
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Anderson, S.F.1
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0032932528
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Tsix, a gene antisense to Xist at the X-inactivation centre
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Lee J.T., Davidow L.S., Warshawsky D. Tsix, a gene antisense to Xist at the X-inactivation centre. Nat. Genet. 21:1999;400-404.
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Lee, J.T.1
Davidow, L.S.2
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Disruption of imprinted X inactivation by parent-of-origin effects at Tsix
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Lee J.T. Disruption of imprinted X inactivation by parent-of-origin effects at Tsix. Cell. 103:2000;17-27.
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Cell
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Lee, J.T.1
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Lee J.T., Lu N. Targeted mutagenesis of Tsix leads to nonrandom X inactivation. Cell. 99:1999;47-57.
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Cell
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Lee, J.T.1
Lu, N.2
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41
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0035030004
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Regulation of imprinted X-chromosome inactivation in mice by Tsix
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•], these papers demonstrate that transcription of Tsix negatively regulates Xist by decreasing the steady-state levels of Xist RNA.
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•], these papers demonstrate that transcription of Tsix negatively regulates Xist by decreasing the steady-state levels of Xist RNA.
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(2001)
Development
, vol.128
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Sado, T.1
Wang, Z.2
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Li, E.4
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Genomic imprinting: Parental influence on the genome
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Reik W., Walter J. Genomic imprinting: parental influence on the genome. Nat. Rev. Genet. 2:2001;21-32.
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Reik, W.1
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Characterization and quantitation of differential Tsix transcripts: Implications for Tsix function
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Shibata S., Lee J.T. Characterization and quantitation of differential Tsix transcripts: implications for Tsix function. Hum. Mol. Genet. 12:2003;125-136.
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Forty years of decoding the silence in X-chromosome inactivation
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Boumil R.M., Lee J.T. Forty years of decoding the silence in X-chromosome inactivation. Hum. Mol. Genet. 10:2001;2225-2232.
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Boumil, R.M.1
Lee, J.T.2
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0034628634
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Ordered assembly of roX RNAs into MSL complexes on the dosage-compensated X chromosome in Drosophila
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Meller V.H., Gordadze P.R., Park Y., Chu X., Stuckenholz C., Kelley R.L., Kuroda M.I. Ordered assembly of roX RNAs into MSL complexes on the dosage-compensated X chromosome in Drosophila. Curr. Biol. 10:2000;136-143.
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