First Author | Matsui J | Year | 2001 |
Journal | Hum Mol Genet | Volume | 10 |
Issue | 13 | Pages | 1393-401 |
PubMed ID | 11440992 | Mgi Jnum | J:70372 |
Mgi Id | MGI:2137124 | Doi | 10.1093/hmg/10.13.1393 |
Citation | Matsui J, et al. (2001) Control of Xist expression for imprinted and random X chromosome inactivation in mice. Hum Mol Genet 10(13):1393-401 |
abstractText | Applying RNA fluorescence in situ hybridization to parthenogenetic embryos with two maternally derived X (X(M)) chromosomes and embryos with X chromosome aneuploidy such as X(P)0 (X(P), paternally derived X chromosome), X(M)X(M)X(P) and X(M)X(M)Y, 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 X(P)-inactivation, whereas in X(P)0 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 X(M)X(P) and X(M)X(M)X(P) 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. |