Effect of Tsix disruption on Xist expression in male ES cells

被引：27
作者：
Sado, T
Li, E
Sasaki, H
机构：
[1] Natl Inst Genet, Div Human Genet, Mishima, Shizuoka 4118540, Japan
[2] Grad Univ Adv Studies, Dept Biosyst Sci, Mishima, Shizuoka, Japan
[3] Grad Univ Adv Studies, Dept Genet, Mishima, Shizuoka, Japan
[4] Massachusetts Gen Hosp E, Cutaneous Biol Res Ctr, Charlestown, MA USA
[5] Massachusetts Gen Hosp E, Cardiobiol Res Ctr, Charlestown, MA USA
[6] Harvard Univ, Sch Med, Dept Dermatol, Charlestown, MA USA
来源：
CYTOGENETIC AND GENOME RESEARCH | 2002年 / 99卷 / 1-4期
关键词：
D O I：
10.1159/000071582
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
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. Copyright (C) 2002 S. Karger AG, Basel.
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页码：115 / 118
页数：4
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