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Xite, X-Inactivation Intergenic Transcription Elements that Regulate the Probability of Choice
Allelic expression differences contribute to phenotypic variation. In X chromosome inactivation (XCI), unfavorable XCI ratios promote X-linked disease penetrance in females. During XCI, one X is randomly silenced by Xist. X chromosome choice is determined by asymmetric expression of Tsix whose antis...
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Published in: | Molecular cell 2003-03, Vol.11 (3), p.731-743 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Allelic expression differences contribute to phenotypic variation. In X chromosome inactivation (XCI), unfavorable XCI ratios promote X-linked disease penetrance in females. During XCI, one X is randomly silenced by
Xist. X chromosome choice is determined by asymmetric expression of
Tsix whose antisense action represses
Xist. Here, we discover a
cis element in the mouse X-inactivation center that regulates
Tsix.
Xite harbors intergenic transcription start sites and DNaseI hypersensitive sites with allelic differences. At the onset of XCI, deleting
Xite downregulates
Tsix in
cis and skews XCI ratios, suggesting that
Xite promotes
Tsix persistence on the active X. Truncating
Xite RNA is inconsequential, indicating that
Xite action does not require intact transcripts. We propose that allele-specific
Xite action promotes
Tsix asymmetry and generates X chromosome inequality. Therefore,
Xite is a candidate for the
Xce, the classical modifier of XCI ratios. |
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ISSN: | 1097-2765 1097-4164 |
DOI: | 10.1016/S1097-2765(03)00063-7 |