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The mouse Xist gene maps to the X inactivation center (Xic) region and is expressed exclusively from the inactive X chromosome. It is thus a candidate gene for the Xic. We show that the onset of Xist expression in mouse development precedes X chromosome inactivation and may therefore be a cause rather than merely a consequence of X inactivation. The earliest Xist expression in morulae and blastocysts is imprinted, resulting in specific expression of the paternal Xist allele. Imprinted Xist expression may thus be the cause of nonrandom inactivation of the paternal X in trophectoderm. Strong Xce alleles can act to reduce the effect of imprinted Xist expression in the trophectoderm. The imprint on Xist expression is lost shortly before gastrulation when random X inactivation occurs. Our data support a direct role for Xist in the initiation of X inactivation.

Original publication

DOI

10.1016/0092-8674(93)90658-d

Type

Journal article

Journal

Cell

Publication Date

29/01/1993

Volume

72

Pages

171 - 182

Keywords

Aging, Alleles, Animals, Base Sequence, Blastocyst, Cell Line, DNA, Ectoderm, Embryo, Mammalian, Embryonic and Fetal Development, Female, Fertilization in Vitro, Gastrula, Gene Expression, Male, Mice, Mice, Inbred Strains, Models, Biological, Molecular Sequence Data, Muridae, Oligodeoxyribonucleotides, Polymerase Chain Reaction, Pregnancy, Testis, X Chromosome