On the other hand, it appears more likely that the A/B transcript is non-coding, as the existence of an endogenous A/B protein is not supported by experimental evidence. Furthermore, similar to other non-coding RNA molecules in the genome, the A/B transcript and/or the exon A/B DMR has an important role in regulating gene expression from GNAS. Unlike the DMRs comprising the promoters of NESP55 and XLαs, the exon A/B DMR has been shown to be a germ-line imprint mark [85]. It has also been shown that this DMR is associated with allele-specific differences in histone modifications consistent with an active paternal (histone acetylation and histone-3 Lys4 methylation) and an inactive maternal (histone-3 Lys9 metyhlation) promoter [42, 87]. In addition, paternal ablation of the A/B DMR results in derepression of the Gsα transcript in those tissues where paternal Gsα expression is normally silenced, such as the renal cortex [81, 88]. Thus, it appears that the non-methylated A/B DMR and/or active A/B transcription is necessary for the tissue-specific paternal silencing of Gsα. Consistent with this finding, maternal exon A/B is unmethylated and
