In order to determine which imprinted genes we could confidently analyze in our study, we identified a panel of loci that showed appropriate imprinting in normal tissue samples, as well as gynogenetic and androgenetic samples. We observed aberrations at many of the examined imprinted genes in a substantial subset of hPSCs; changes at some loci arose during reprogramming and others over time in culture. Very few studies have addressed potential causes of aberrant imprinting in hPSCS (such as culture conditions or derivation methods), although a recent study comparing the hESC line WA09 and six isogenic WA09-derived hiPSC lines reported that imprinting of NNAT (as well as XCI) was specifically lost in hiPSCs compared to hESCs (Teichroeb et al., 2011). While we identified NNAT as one of the genes with hPSC-specific variability in DNA methylation (Figure 1B and Table S2B), none of the observed variations were specific to hESCs or hiPSCs, and none of the 20 CpG sites in the promoter region of NNAT interrogated by the 27K and 450K DNA Methylation array passed our imprinted site filters. Using linear regression,
