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Molecular and Cellular Biology, October 2006, p. 7167-7177, Vol. 26, No. 19
0270-7306/06/$08.00+0     doi:10.1128/MCB.00810-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Hematopoietic Precursor Cells Transiently Reestablish Permissiveness for X Inactivation{dagger}

Fabio Savarese,1 Katja Flahndorfer,1 Rudolf Jaenisch,2 Meinrad Busslinger,1 and Anton Wutz1*

Research Institute of Molecular Pathology, Vienna Biocenter, Dr. Bohr-Gasse 7, 1030 Vienna, Austria,1 Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge Massachusetts 021422

Received 8 May 2006/ Returned for modification 5 June 2006/ Accepted 19 July 2006

Xist is the trigger for X inactivation in female mammals. The long noncoding Xist RNA localizes along one of the two female X chromosomes and initiates chromosome-wide silencing in the early embryo. In differentiated cells, Xist becomes dispensable for the maintenance of the inactive X, and its function for initiation of silencing is lost. How Xist mediates gene repression remains an open question. Here, we use an inducible Xist allele in adult mice to identify cells in which Xist can cause chromosome-wide silencing. We show that Xist has the ability to initiate silencing in immature hematopoietic precursor cells. In contrast, hematopoietic stem cells and mature blood cells are unable to initiate ectopic X inactivation. This indicates that pathways critical for silencing are transiently activated in hematopoietic differentiation. Xist-responsive cell types in normal female mice show a change of chromatin marks on the inactive X. However, dosage compensation is maintained throughout hematopoiesis. Therefore, Xist can initiate silencing in precursors with concomitant maintenance of dosage compensation. This suggests that Xist function is restricted in development by the limited activity of epigenetic pathways rather than by a change in the responsiveness of chromatin between embryonic and differentiated cell types.

* Corresponding author. Mailing address: Research Institute of Molecular Pathology, Vienna Biocenter, Dr. Bohr-Gasse 7, 1030 Vienna, Austria. Phone: 43 1 797 30 521. Fax: 43 1 798 93 70. E-mail: wutz{at}imp.univie.ac.at.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, October 2006, p. 7167-7177, Vol. 26, No. 19
0270-7306/06/$08.00+0     doi:10.1128/MCB.00810-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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  • Chow, J. C., Hall, L. L., Baldry, S. E. L., Thorogood, N. P., Lawrence, J. B., Brown, C. J. (2007). Inducible XIST-dependent X-chromosome inactivation in human somatic cells is reversible. Proc. Natl. Acad. Sci. USA 104: 10104-10109 [Abstract] [Full Text]  


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