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The onset of X inactivation is preceded by a marked increase in the level of Xist RNA. Here we demonstrate that increased stability of Xist RNA is the primary determinant of developmental up-regulation. Unstable transcript is produced by both alleles in XX ES cells and in XX embryos prior to the onset of random X inactivation. Following differentiation, transcription of unstable RNA from the active X chromosome allele continues for a period following stabilization and accumulation of transcript on the inactive X allele. We discuss the implications of these findings in terms of models for the initiation of random and imprinted X inactivation.

Type

Journal article

Journal

Cell

Publication Date

03/10/1997

Volume

91

Pages

99 - 107

Keywords

Alleles, Animals, Blastocyst, Cell Differentiation, Cells, Cultured, Dactinomycin, Dosage Compensation, Genetic, Female, Gene Expression Regulation, Male, Mice, Models, Genetic, Nucleic Acid Synthesis Inhibitors, RNA, Long Noncoding, RNA, Messenger, RNA, Untranslated, Stem Cells, Transcription Factors, Transcription, Genetic