International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)

I35. X Chromosome Inactivation in XX Androgeneticmouse Embryos Surviving Implantation

Ikuhiro, Okamoto1, Seong-Seng, Tan3 and Nobuo, Takagi1,2
1Division of Bioscience, Graduate School of Environmental Earth Science and
Research Center for Molecular Genetics, Hokkaido University, Sapporo 0600810, Japan
3Developmental Biology Laboratory, Howard Florey Institute, The University of Melbourne, Parkville, Victoria, Austraria

Using genetic and cytogenetic markers, we assessed early development and X-chromosome inactivation in XX mouse androgenones produced by pronuclear transfer. Contrary to the current view, XX androgenones are capable of surviving to embryonic day 7.5, achieving basically random X inactivation in all tissues including those derived from the trophectoderm and primitive endoderm that are characterized by paternal X-inactivation in fertilized embryos. This finding supports the hypothesis that in fertilized female embryos the maternal X chromosome remains active until the blastocyst stage because of a rigid imprint that prevents inactivation, whereas the paternal X is preferentially inactivated in extraembryonic tissues due to lack of such imprint. In spite of random X inactivation in XX androgenones, FISH analyses revealed expression of stable Xist RNA from every X chromosome in XX and XY androgenonetic embryos from the 4-cell to morula stage. Although the occurrence of inappropriate X-inactivation was further suggested by the finding that Xist continues ectopic expression in a proportion of cells from XX and XY androgenones at the blastocyst and the early egg cylinder stage, a replication banding study failed to provide positive evidence for inappropriate X-inactivation at E6.5.

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