caa a22 4500 445861207 CHVBK 20180317145443.0 cr unu---uuuuu 170323e20110801xx s 000 0 eng 10.1007/s00439-011-1024-7 doi (NATIONALLICENCE)springer-10.1007/s00439-011-1024-7 X-inactivation and X-reactivation: epigenetic hallmarks of mammalian reproduction and pluripotent stem cells [Elektronische Daten] [Bernhard Payer, Jeannie Lee, Satoshi Namekawa] X-chromosome inactivation is an epigenetic hallmark of mammalian development. Chromosome-wide regulation of the X-chromosome is essential in embryonic and germ cell development. In the male germline, the X-chromosome goes through meiotic sex chromosome inactivation, and the chromosome-wide silencing is maintained from meiosis into spermatids before the transmission to female embryos. In early female mouse embryos, X-inactivation is imprinted to occur on the paternal X-chromosome, representing the epigenetic programs acquired in both parental germlines. Recent advances revealed that the inactive X-chromosome in both females and males can be dissected into two elements: repeat elements versus unique coding genes. The inactive paternal X in female preimplantation embryos is reactivated in the inner cell mass of blastocysts in order to subsequently allow the random form of X-inactivation in the female embryo, by which both Xs have an equal chance of being inactivated. X-chromosome reactivation is regulated by pluripotency factors and also occurs in early female germ cells and in pluripotent stem cells, where X-reactivation is a stringent marker of naive ground state pluripotency. Here we summarize recent progress in the study of X-inactivation and X-reactivation during mammalian reproduction and development as well as in pluripotent stem cells. Springer-Verlag, 2011 Payer Bernhard Department of Genetics, Harvard Medical School, Boston, MA, USA aut Lee Jeannie Department of Genetics, Harvard Medical School, Boston, MA, USA aut Namekawa Satoshi Division of Reproductive Sciences, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA aut Human Genetics Springer-Verlag 130/2(2011-08-01), 265-280 0340-6717 130:2<265 2011 130 439 https://doi.org/10.1007/s00439-011-1024-7 text/html Onlinezugriff via DOI 1 review-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00439-011-1024-7 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Payer Bernhard Department of Genetics, Harvard Medical School, Boston, MA, USA aut NATIONALLICENCE 700 1- Lee Jeannie Department of Genetics, Harvard Medical School, Boston, MA, USA aut NATIONALLICENCE 700 1- Namekawa Satoshi Division of Reproductive Sciences, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA aut NATIONALLICENCE 773 0- Human Genetics Springer-Verlag 130/2(2011-08-01), 265-280 0340-6717 130:2<265 2011 130 439 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer