Effect of Tsix disruption on Xist expression in male ES cells

T. Sado, E. Li, H. Sasaki

研究成果: ジャーナルへの寄稿学術誌査読

26 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)115-118
ページ数4
ジャーナルCytogenetic and Genome Research
99
1-4
DOI
出版ステータス出版済み - 2002
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 分子生物学
  • 遺伝学
  • 遺伝学(臨床)

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