X chromosome inactivation
Effect of Tsix disruption on Xist expression in male ES cellsSado T.a,b,c · Li E.d,e · Sasaki H.a,c
aDivision of Human Genetics, National Institute of Genetics, Departments of bBiosystems Science and cGenetics, The Graduate University for Advanced Studies, Mishima (Japan); dCutaneous Biology Research Center and Cardiobiology Research Center, Massachusetts General Hospital-East, eDepartment of Dermatology, Harvard Medical School, Charlestown MA (USA)
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Article / Publication Details
Xist and its antisense partner, Tsix, encode non-coding RNAs and play key roles in X chromosome inactivation. Targeted disruption of Tsix causes ectopic expression of Xist in the extraembryonic tissues upon maternal transmission, which subsequently results in embryonic lethality due to inactivation of both X chromosomes in females and a single X chromosome in males. Tsix, therefore, plays a crucial role in maintaining the silenced state of Xist in cis and regulates the imprinted X inactivation in the extraembryonic tissues. In this study, we examined the effect of Tsix disruption on Xist expression in the embryonic lineage using embryonic stem (ES) cells as a model system. Upon differentiation, Xist is ectopically activated in a subset of the nuclei of male ES cells harboring the Tsix-deficient X chromosome. Such ectopic expression, however, eventually ceased during prolonged culture. It is likely that surveillance by the X chromosome counting mechanism somehow shuts off the ectopic expression of Xist before inactivation of the X chromosome.
© 2002 S. Karger AG, Basel
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