Published online before print June 18, 2002, 10.1073/pnas.132468999
Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 13, 8677-8682, June 25, 2002
http://www.pnas.org/cgi/doi/10.1073/pnas.132468999


"An Ectopic Human XIST Gene Can Induce Chromosome Inactivation in Post-differentiation Human HT-1080 Cells".

Lisa L. Hall 1, Meg Byron 1, Kosuke Sakai 2, Laura Carrel 2, Huntington F. Willard 2, and Jeanne B. Lawrence 1, @,

1 Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655; and        2 Department of Genetics, Case Western Reserve University School of Medicine, Cleveland, OH 44106

@ To whom reprint requests should be addressed. E-mail:   jeanne.lawrence@umassmed.edu



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 post-differentiation 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 post-differentiation 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.



Additional References:

1. Wutz A, Rasmussen TP, and Jaenisch R, "Chromosomal Silencing and Localization are Mediated by Different Domains of Xist RNA".

2. Luikenhuis S, Wutz A, and Jaenisch R, "Antisense Transcription Through the Xist Locus Mediates Tsix Function in Embryonic Stem Cells".

3. Stavropoulos N, Lu N, and Lee, JT, "A Functional Role for Tsix Transcription in Blocking Xist RNA Accumulation but Not in X-Chromosome Choice".

4. Kelley RL, and Kuroda MI, "The Role of Chromosomal RNAs in Marking the X for Dosage Compensation".

5. Wutz A, and Jaenisch R, "A Shift from Reversible to Irreversible X Inactivation is Triggered during ES Cell Differentiation".

6. Frenster JH, "Ultrastructural Probes of Active DNA Sites, and the RNA Activators of DNA".



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