High impact information on Jarid1c

• Escape from X inactivation of Smcx is preceded by silencing during mouse development [1].
• In vitro and in vivo studies show that Xe169 is expressed from both the active and the inactive X chromosomes [2].
• We have recently identified Smcy, a ubiquitously expressed gene, in this region and its X-chromosome homologue, Smcx [3].
• To understand how gene expression patterns are established on the inactive X chromosome during development, we have studied the murine gene Smcx, which is expressed from both the active and inactive mouse X chromosomes [4].
• We found that long terminal repeats (LTRs) were decreased in the human domain of escape, but not in the majority of the conserved mouse region adjacent to Smcx in which genes were subject to X inactivation, suggesting that these repeats might be excluded from escape domains to prevent spreading of silencing [5].

Biological context of Jarid1c

• The different patterns of replacement and silent substitutions within Jarid1d and Jarid1c may be a result of evolutionary mechanisms that are particularly strong on the Y chromosome because of its unique properties [6].

Analytical, diagnostic and therapeutic context of Jarid1c

• In situ hybridization also showed that the Smcx (Xe169) gene maps near Sb1.8 in band F [7].
• Xe169 was assigned to band F2/F3 on the mouse X chromosome by fluorescent in situ hybridization and Southern analysis indicates that the gene is located outside the pseudoautosomal region [2].
• Sequence analysis and functional characterization of the mouse Smcx promoter did not reveal any obvious unique features that would explain the difference in the behavior of this gene on the inactive X compared with other nearby genes [8].

References