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Epigenetic mechanisms restrict the expression of imprinted genes to one parental allele in diploid cells. At the  Igf2r/Air  imprinted cluster on mouse chromosome 17, paternal-specific expression of the  Air  noncoding RNA has been shown to silence three genes in  cis :  Igf2r, Slc22a2 , and  Slc22a3 . By an unbiased mapping of DNase I hypersensitive sites (DHS) in a 192-kb region flanking  Igf2r  and  Air , we identified 21 DHS, of which nine mapped to evolutionarily conserved sequences. Based on the hypothesis that silencing effects of  Air  would be directed towards  cis  regulatory elements used to activate genes, DHS are potential key players in the control of imprinted expression. However, in this 192-kb region only the two DHS mapping to the  Igf2r  and  Air  promoters show parental specificity. The remaining 19 DHS were present on both parental alleles and, thus, have the potential to activate  Igf2r  on the maternal allele and  Air  on the paternal allele. The possibility that the  Igf2r  and  Air  promoters share the same  cis -acting regulatory elements, albeit on opposite parental chromosomes, was supported by the similar expression profiles of  Igf2r  and  Air  in vivo. These results refine our understanding of the onset of imprinted silencing at this cluster and indicate the  Air  noncoding RNA may specifically target silencing to the  Igf2r  promoter.

Long-range DNase I hypersensitivity mapping reveals the imprinted Igf2r and Air promoters share cis-regulatory elements