Molecular links between x-inactivation and autosomal imprinting: X-inactivation as a driving force for the evolution of imprinting?
TLDR
The need for X-linked dosage compensation was a major driving force in the evolution of genomic imprinting in mammals and it is proposed that imprinting was first fixed on the X chromosome for XCI and subsequently acquired by autosomes.About:
This article is published in Current Biology.The article was published on 2003-03-18 and is currently open access. It has received 117 citations till now. The article focuses on the topics: Genomic imprinting & Imprinting (psychology).read more
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Analysis of the Vertebrate Insulator Protein CTCF-Binding Sites in the Human Genome
Tae Hoon Kim,Ziedulla Abdullaev,Andrew D. Smith,Keith A. Ching,Dmitri Loukinov,Roland Green,Michael Q. Zhang,Victor V. Lobanenkov,Bing Ren +8 more
TL;DR: 13,804 CTCF-binding sites in potential insulators of the human genome are described, discovered experimentally in primary human fibroblasts and fit to a consensus motif highly conserved and suitable for predicting possible insulators driven by CTCf in other vertebrate genomes.
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Epigenetics: definition, mechanisms and clinical perspective.
TL;DR: The complete array of human assisted reproductive technology (ART), starting from ovarian hormonal stimulation to embryo uterine transfer, could have a profound impact on the epigenetic state of human in vitro produced individuals.
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Evolution of the mammalian transcription factor binding repertoire via transposable elements
Guillaume Bourque,Bernard Leong,Vinsensius B. Vega,Xi Chen,Yen Ling Lee,Kandhadayar G. Srinivasan,Joon-Lin Chew,Yijun Ruan,Chia-Lin Wei,Huck-Hui Ng,Edison T. Liu +10 more
TL;DR: It is established that these repeat-associated binding sites (RABS) have been associated with significant regulatory expansions throughout the mammalian phylogeny and that transposable elements play an important role in expanding the repertoire of binding sites.
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X chromosome dosage compensation: how mammals keep the balance
Bernhard Payer,Jeannie T. Lee +1 more
TL;DR: Various facets of the ever-expanding field of mammalian dosage compensation are reviewed and its evolutionary, developmental, and mechanistic components are discussed.
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Postmeiotic Sex Chromatin in the Male Germline of Mice
Satoshi H. Namekawa,Peter J. Park,Li-Feng Zhang,James E. Shima,John R. McCarrey,Michael D. Griswold,Jeannie T. Lee +6 more
TL;DR: In this article, a comprehensive X-expression profile during mouse spermatogenesis was established, and it was shown that the X and Y chromosomes occupied a novel compartment in the postmeiotic Spermatid and adopted a non-Rabl configuration.
References
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Targeted mutation of the DNA methyltransferase gene results in embryonic lethality.
TL;DR: Results indicate that while a 3-fold reduction in levels of genomic m5C has no detectable effect on the viability or proliferation of ES cells in culture, a similar reduction of DNA methylation in embryos causes abnormal development and embryonic lethality.
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Gene Action in the X -chromosome of the Mouse ( Mus musculus L.)
TL;DR: Ohno and Hauschka1 showed that in female mice one chromosome of mammary carcinoma cells and of normal diploid cells of the ovary, mammary gland and liver was heteropyKnotic and suggested that the so-called sex chromatin was composed of one heteropyknotic X-chromosome.
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Role of Histone H3 Lysine 27 Methylation in Polycomb-Group Silencing
Ru Cao,Liangjun Wang,Hengbin Wang,Li Xia,Hediye Erdjument-Bromage,Paul Tempst,Richard S. Jones,Yi Zhang +7 more
TL;DR: The purification and characterization of an EED-EZH2 complex, the human counterpart of the Drosophila ESC-E(Z) complex, is reported, and it is demonstrated that the complex specifically methylates nucleosomal histone H3 at lysine 27 (H3-K27).
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Genomic imprinting: parental influence on the genome
TL;DR: The study of imprinting provides new insights into epigenetic gene modification during development, and is thought to influence the transfer of nutrients to the fetus and the newborn from the mother.
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Role for DNA methylation in genomic imprinting
TL;DR: It is demonstrated that a normal level of DNA methylation is required for controlling differential expression of the paternal and maternal alleles of imprinted genes in mutant mice that are deficient in DNA methyltransferase activity.