Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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




Journal article



Publication Date





171 - 182


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