Nissim Benvenisty, from Hebrew University of Jerusalem, discussed epigenetic regulation of stem cells. By generating parthogenetic hiPSCs from female teratomas that harbor two sets of maternal chromosomes, his group was able to identify novel imprinted genes, including many miRNAs (Stelzer et al., 2011). Rather than observing decreased expression in all paternally expressed genes in parthogenetic hiPSCs, he reported that about half of the known paternally expressed genes were unexpectedly not downregulated. Two classes of imprinted genes were resolved: the first was downregulated in all parthenogenetic cell types and included classical imprinted genes such as PEG10, whereas the second was not downregulated in some or all examined parthenogenetic cell types and showed overlapping imprinted and non-imprinted isoforms; this resulted from expression from two promoters, only one of which was imprinted (Stelzer et al., 2015). In this context, Benvenisty considered whether parthenogenetic hiPSCs could be used to model epigenetic human disorders such as the neurological Prader-Willi Syndrome (PWS), which results from maternal uniparental disomy of chromosome 15. Characterization of the parthogenetic PSCs and iPSCs from PWS patients revealed specific maternal expression of
