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Human Molecular Genetics, 2001, Vol. 10, No. 13 1393-1401
© 2001 Oxford University Press

Control of Xist expression for imprinted and random X chromosome inactivation in mice

Junko Matsui, Yuji Goto and Nobuo Takagi+

Graduate School of Environmental Earth Sciences, Hokkaido University, North 10, West 5, Kita-ku, Sapporo 060-0810, Japan

Applying RNA fluorescence in situ hybridization to parthenogenetic embryos with two maternally derived X (XM) chromosomes and embryos with X chromosome aneuploidy such as XP0 (XP, paternally derived X chromosome), XMXMXP and XMXMY, we studied the control of Xist/Tsix expression for silencing the entire X chromosome in mice. The data show that the paternally derived Xist allele is highly expressed in every cell of the embryo from the 4-cell stage onward, irrespective of the number of X chromosomes in a diploid cell. The high level of Xist transcription is maintained in non-epiblast cells culminating in XP-inactivation, whereas in XP0 embryos it is terminated by the blastocyst stage, probably as a result of counting the number of X chromosomes in a cell occurring at the morula/blastocyst stage. Xist is also down-regulated in epiblast cells of XMXP and XMXMXP embryos to make X-inactivation random. In epiblast cells, Xist seems to be up-regulated after counting and random choice of the future inactive X chromosome(s). Although the maternal Xist allele is never activated in fertilized embryos before implantation, some parthenogenetic embryos show Xist up-regulation in a proportion of cells. These and other data reported earlier suggest that imprinted X-inactivation in non-epiblast tissues of rodents had been derived from the random X-inactivation system.

+ To whom correspondence should be addressed. Tel: +81 11 706 4524; Fax: +81 11 706 4524; Email: ntakagi@ees.hokudai.ac.jp


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