Effect of TSIX disruption on XIST expression in male ES cells.
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.[1]References
- Effect of TSIX disruption on XIST expression in male ES cells. Sado, T., Li, E., Sasaki, H. Cytogenet. Genome Res. (2002) [Pubmed]
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