a1 Research Center for Molecular Genetics and Division of Biological Science, Graduate School of Environmental Earth Science, Hokkaido University, Sapporo, Japan
a2 Institut für Säugetiergenetik, Forschungcentrum für Umwelt und Gesundheit Neuherberg, 85758 Oberschleissheim, Germany
To examine the effects of X-chromosome imprinting during early mouse embryogenesis, we attempted to produce XM0, Xp0, XMXMY, XMXPY and XMXMXP (where XM and Xp stand for the maternally and the paternally derived X chromosome, respectively) making use of mouse strains bearing the translocation Rb(X.2)2Ad and the inversion In(X)1H. Unlike XMXPY embryos, XMXMY and XMXMXP conceptuses suffered from severe growth retardation or abnormal development characterized by deficient extra-embryonic structures at 6.5–7.5 days post coitum (dpc). A cytogenetic study suggested that two XM chromosomes remaining active in certain non-epiblast cells were responsible for the serious developmental abnormality found in these embryos disomic for XM. Although matings involving females heterozygous for Rb(X.2)2Ad hinted at the paucity of XP0 embryos relative to those having the complementary karyotype of XMXMXP, further study of embryos from matings between females heterozygous for In(X)1H and Rb2Ad males did not substantiate this observation. Thus, the extensive peri-implantation loss of XP0 embryos shown by Hunt (1991) may be confined to XO mothers. Taken together, this study failed to reveal a parentally imprinted X-linked gene essential for early mouse embryogenesis other than the one most probably corresponding to the X-chromosome inactivation centre.
(Received April 13 1993)
(Revised June 11 1993)
c1 Corresponding author.