NDLI: An ectopic human XIST gene can induce chromosome inactivation in postdifferentiation human HT-1080 cells.

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An ectopic human XIST gene can induce chromosome inactivation in postdifferentiation human HT-1080 cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Carrel, Laura Lawrence, Jeanne B. Hall, Lisa L. Byron, Meg Sakai, Kosuke Willard, Huntington F.
Description	Author Affiliation: Hall LL ( Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA.);
Abstract	It has been believed that XIST RNA requires a discrete window in early development to initiate the series of chromatin-remodeling events that form the heterochromatic inactive X chromosome. Here we investigate four adult male HT-1080 fibrosarcoma cell lines expressing ectopic human XIST and demonstrate that these postdifferentiation cells can undergo chromosomal inactivation outside of any normal developmental context. All four clonal lines inactivated the transgene-containing autosome to varying degrees and with variable stability. One clone in particular consistently localized the ectopic XIST RNA to a discrete chromosome territory that exhibited striking hallmarks of inactivation, including long-range transcriptional inactivation. Results suggest that some postdifferentiation cell lines are capable of de novo chromosomal inactivation; however, long-term retention of autosomal inactivation was less common, which suggests that autosomal inactivation may confer a selective disadvantage. These results have fundamental significance for understanding genomic programming in early development.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	13
Volume Number	99
Language	English
Publisher	National Academy of Sciences
Publisher Date	2002-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Differentiation Genetics Chromosomes, Human RNA, Untranslated Transcription Factors Acetylation Gene Silencing In Situ Hybridization, Fluorescence Microscopy, Fluorescence RNA RNA, Long Noncoding Transcription, Genetic Tumor Cells, Cultured Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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