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J. Cell Biol.,
Volume 142, Number 1, July 13, 1998 13-23
* Department of Cell Biology, University of Massachusetts Medical Center, Worcester, Massachusetts 01655; and These studies address whether XIST RNA is
properly localized to the X chromosome in somatic
cells where human XIST expression is reactivated, but
fails to result in X inactivation (Tinker, A.V., and C.J.
Brown. 1998. Nucl. Acids Res. 26:2935-2940). Despite a
nuclear RNA accumulation of normal abundance and
stability, XIST RNA does not localize in reactivants or
in naturally inactive human X chromosomes in mouse/
human hybrid cells. The XIST transcripts are fully stabilized despite their inability to localize, and hence
XIST RNA localization can be uncoupled from stabilization, indicating that these are separate steps controlled by distinct mechanisms. Mouse Xist RNA
tightly localized to an active X chromosome, demonstrating for the first time that the active X chromosome in somatic cells is competent to associate with Xist
RNA. These results imply that species-specific factors,
present even in mature, somatic cells that do not normally express Xist, are necessary for localization. When
Xist RNA is properly localized to an active mouse X
chromosome, X inactivation does not result. Therefore, there is not a strict correlation between Xist localization
and chromatin inactivation. Moreover, expression, stabilization, and localization of Xist RNA are not sufficient
for X inactivation. We hypothesize that chromosomal
association of XIST RNA may initiate subsequent developmental events required to enact transcriptional silencing.
Department
of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada V6T1Z3
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