Micromanipulating dosage compensation: understanding X-chromosome inactivation through nuclear transplantation.
Nuclear transfer (NT) studies have provided insight into the functional importance of epigenetic alteration of the X chromosomes during X-inactivation. Uniparental embryos created by NT have been informative as to the time and location at which the imprint controlling extraembryonic X-inactivation is established. Experiments with female somatic cells, have demonstrated that the inactive X chromosome (Xi) is reactivated after NT, leading to random X-inactivation in the embryonic lineages of cloned embryos. However, in the extraembryonic lineages of clones, epigenetic information from the donor cell nucleus persists, leading to preferential inactivation of the donor cell's inactive X in the placenta of cloned animals. These results suggest epigenetic information established during embryonic X-inactivation is functionally equivalent to the gametic imprint.
Eggan
Kevin
K
Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, MA 02142, USA.
Jaenisch
Rudolf
R
D000818:Animals; D002467:Cell Nucleus / Q000235:genetics*; D004303:Dosage Compensation, Genetic; D004622:Embryo, Mammalian / Q000166:cytology; D005314:Embryonic and Fetal Development / Q000235:genetics; D005260:Female; D018507:Gene Expression Regulation, Developmental; D018392:Genomic Imprinting; D008297:Male; D051379:Mice; D009865:Oocytes / Q000166:cytology; D033581:Stem Cell Transplantation; D013234:Stem Cells / Q000166:cytology*; D014960:X Chromosome / Q000235:genetics*