High impact information on Xite

• We propose that allele-specific Xite action promotes Tsix asymmetry and generates X chromosome inequality [1].
• Xite, X-inactivation intergenic transcription elements that regulate the probability of choice [1].
• Xite harbors intergenic transcription start sites and DNaseI hypersensitive sites with allelic differences [1].
• Genetic control of X chromosome inactivation in mice: definition of the Xce candidate interval [2].
• Subsequent analysis of recombinant chromosomes allowed for the establishment of a maximum 1.85-Mb candidate region for the Xce locus [2].

Biological context of Xite

• Differential methylation of Xite and CTCF sites in Tsix mirrors the pattern of X-inactivation choice in mice [3].
• Because the pattern of DNA methylation mirrors events of X-inactivation, we propose that differential methylation of DMDs in Tsix and Xite constitute a primary mark for epigenetic regulation [3].
• These experiments revealed the intergenic transcription element Xite as an enhancer of Tsix and the repeat element DXPas34 as a component of the bipartite enhancer [4].
• Here, a mouse knockout and transgenic analysis identified DNA sequences within the noncoding Tsix and Xite genes as numerators [5].
• In this report, we used quantitative trait locus (QTL) mapping strategies to define the minimal Xce candidate interval [2].

Other interactions of Xite

• Thus, Tsix and Xite function both in cis and in trans [6].
• X inactivation is known to be regulated in cis by Xite, Tsix, and Xist, but in principle the two Xs must also be regulated in trans to ensure mutually exclusive silencing [6].

References