[Comparative organization and the origin of noncoding regulatory RNA genes from X-chromosome inactivation center of human and mouse].
After the radiation of primates and rodents, the evolution of X-chromosome inactivation centers in human and mouse (XIC/Xic) followed two different directions. Human XIC followed the pathway towards transposon accumulation (the repeat proportion in the center constitutes 72%), especially LINEs, which prevail in the center. On the contrary, mouse Xic eliminated long repeats and accumulated species-specific SIN Es (the repeat proportion in the center constitutes 35%). The mechanism underlying inactivation of one of the X chromosomes in female mammals appeared on the basis of trasnsposons. The key gene of the inactivation process, XIST/Xist, similarly to other long noncoding RNA genes, like TSIX/Tsix, JPX/Jpx, and FTX/Ftx, was formed with the involvement of different transposon sequences. Furthermore, two clusters ofmicroRNA genes from inactivation center originated from L2 [1]. In mouse, one of such clusters has been preserved in the form of microRNA pseudogenes. Thus, long ncRNA genes and microRNAs appeared during the period of transposable elements expansion in this locus, 140 to 105 Myr ago, after the radiation of marsupials and placental mammal lineages.
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Kolesnikov
E A
EA
Elisafenko
D000818:Animals; D041321:Chromosomes, Human, X / Q000235:genetics*; D004251:DNA Transposable Elements / Q000235:genetics*; D019143:Evolution, Molecular; D005260:Female; D006801:Humans; D051379:Mice; D035683:MicroRNAs / Q000235:genetics*; D013045:Species Specificity; D049951:X Chromosome Inactivation / Q000235:genetics*
D004251:DNA Transposable Elements; D035683:MicroRNAs