Effect of Tsix disruption on Xist expression in male ES cells

T. Sado, E. Li, H. Sasaki

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)115-118
Number of pages4
JournalCytogenetic and Genome Research
Volume99
Issue number1-4
DOIs
Publication statusPublished - Dec 1 2002
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Genetics(clinical)

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