International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)

Table of Contents * Genes, Physical Mapping and Sequencing * Gene Identification * Bioinformatics * Common Resources * RIKEN Session * Functional Genomics * Complex Traits * Mutagenesis * Developmental Genetics and Differentiation * Verne Chapman Memorial Lecture I and II

I35. X Chromosome Inactivation in XX Androgeneticmouse Embryos Surviving Implantation

Ikuhiro, Okamoto¹, Seong-Seng, Tan³ and Nobuo, Takagi^1,2
1Division of Bioscience, Graduate School of Environmental Earth Science and
²Research 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.