Effect of Tsix disruption on Xist expression in male ES cells

• Published in: Cytogenetic and Genome Research Vol. 99; no. 1-4; pp. 115 - 118
• Main Authors: Sado, T., Li, E., Sasaki, H.
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.01.2002
• Subjects: Animals; Cell Line; Embryo, Mammalian - cytology; Embryo, Mammalian - metabolism; Gene Expression Regulation; In Situ Hybridization, Fluorescence - methods; Male; Mice; Mutation; Reverse Transcriptase Polymerase Chain Reaction; RNA - genetics; RNA - metabolism; RNA, Long Noncoding; RNA, Untranslated - genetics; Stem Cells - cytology; Stem Cells - metabolism; Transcription Factors - genetics; X chromosome inactivation
• ISBN: 9783805576376; 3805576374
• ISSN: 1424-8581; 1424-859X
• DOI: 10.1159/000071582

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.