Several studies have demonstrated that the expression of Gsα in most fetal and adult tissues is biallelic, consistent with the absence of differential methylation at its promoter [36-39]. However, in some human and mouse tissues, Gsα expression is predominantly maternal, i.e. paternal Gsα expression is silenced. For example, in the renal cortex, mice with paternal disruption of Gnas exon 2 exhibit Gsα mRNA and protein levels that are similar to those seen in wild-type littermates, whereas mice with maternal disruption of Gnas exon 2 are nearly devoid of Gsα mRNA and protein [40], indicating that renal cortical Gsα expression is derived mostly from the maternal allele. This monoallelic, parent-of-origin specific Gsα expression occurs in a tissue-specific manner, as both mice with the maternal disruption and mice with the paternal disruption show Gsα levels in the renal medulla that are about 50% of the levels seen in wild-type littermates [40]. Similar findings have been reported recently in mice heterozygous for either paternal or maternal disruption of Gnas exon 1, and these studies additionally demonstrated that Gsα expression is also predominantly maternal
