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Developmentally regulated changes in stability of Xist RNA can be attributed to a promoter switch prompting stable and unstable RNA isoforms. Stable Xist RNA comes from the previously identified promoter or from a unique promoter situated 1.5 kb further downstream, while unstable Xist RNA comes from a second novel promoter situated 6.5 kb upstream. It has been shown that promoter switching controls Xist RNA stability at the onset of random and imprinted X inactivation. It has also been shown that imprinted Xist expression takes place as a result of activation of P1/P2 on the Xp allele.

Modulation of Xist RNA was studied to identify its effects on the developmental up-regulation of the X transcript. Results show that up-regulation of Xist RNA marks the beginning of X inactivation due to the increased stability of the transcript it has caused. However, an unstable transcript is caused by the inhibition of the Xist allele such as in the XX ES cells and in XX embryos which also occurs at the onset of X inactivation.

Xist The propagation of X chromosome inactivation is thought to be mediated by the cis-limited spreading of the non-protein coding transcript. In this report we have investigated the localization of Xist RNA on rodent metaphase chromosomes. We show that Xist RNA exhibits a banded pattern on the inactive X and is excluded from regions of constitutive heterochromatin. The banding pattern suggests a preferential association with gene-rich, G-light regions. Analysis of X:autosome rearrangements revealed that restricted propagation of X inactivation into cis-linked autosomal material is reflected by a corresponding limited spread of Xist RNA. We discuss these results in the context of models for the function of Xist RNA in the propagation of X inactivation. [ABSTRACT FROM AUTHOR]