During @entity1 dosage compensation, one of two X-chromosomes in female cells is inactivated. The choice of which X is silenced can be imprinted or stochastic. Although genetic loci influencing the choice decision have been identified, the primary marks for imprinting and random selection remain undefined. Here, we examined the role of DNA methylation, a mechanism known to regulate imprinting in autosomal loci, and sought to determine whether differential methylation on the two Xs might predict their fates. To identify @entity4998 ( @entity4998 ) at the X-inactivation center, we used @entity9736 sequencing and methylation-sensitive restriction enzyme analyses. We found @entity4998 in @entity69510 and @entity70249 , two genes previously shown to influence choice. Interestingly, the @entity4998 in @entity69510 lie within @entity20465 binding sites. Allelic methylation differences occur in gametes and are erased in embryonic stem cells carrying two active Xs. Because the pattern of DNA methylation mirrors events of X-inactivation, we propose that differential methylation of @entity4998 in @entity69510 and @entity70249 constitute a primary mark for epigenetic regulation. The discovery of @entity4998 in @entity20465 sites draws further parallels between X-inactivation and autosomal imprinting.

Differential methylation of @entity70249 and @entity20465 sites in XXXX mirrors the pattern of X-inactivation choice in mice.

@entity1 :: ('9606', 'Species') :: ['mammalian'] @entity70249 :: ('619209(Tax:10090)', 'Gene') :: ['Xite'] @entity4998 :: ('MESH:D012734', 'Disease') :: ['differentially methylated domains', 'DMDs'] @entity9736 :: ('MESH:C042345', 'Chemical') :: ['bisulfite'] @entity20465 :: ('13018(Tax:10090)', 'Gene') :: ['CTCF'] @entity69510 :: ('22097(Tax:10090)', 'Gene') :: ['Tsix']
@entity69510 :: (22097(Tax:10090),Gene) :: ['Tsix']
