Mouse parthenogenetic embryonic stem cells(mesPGESCs)are derived from pre-implantation embryos that developed in the absence of sperm. Because of their exclusively maternal chromosome constituent, these cells are an invaluable tool for studying the role of imprinting and epigenetics in development and differentiation. It has been suggested that when these cells are induced to differentiate, they form cell derivatives from the three germ layers with a preference towards ectoderm at the expense of endoderm and mesoderm. This phenomenon is in part, attributed to the monoparental origin of the cells, which results in deregulation of imprinted genes such as H19, a paternally imprinted gene (i.e. maternally expressed) encoding an untranslated mRNA necessary for normal embryonic development. We derived mesPGESC lines from Rosa 26 strain of mice and found H19 upregulated more than four folds in PGESCs compare to control cell line. We hypothesized that by modulating H19 gene expression we could achieve a more homogeneous cell differentiation of mesPGESCs in a manner similar to that of biparental mouse ES cells (mesBPESCs). We have also aimed to develop a method to quantify the abundance of the tissue derivatives of the three main germ layers in teratomas. Our results show that teratomas derived from mesPGESCs exhibit low abundance of endoderm and mesoderm derivatives, muscle in particular, which coincides with over-expression of H19 and low expression of muscle specific genes such as Myf5, Myf6 and MyoD. We show that this phenotype can be reversed by retroviral mediated silencing of H19 gene expression in mesPGESCs. These results suggest that PGESCs, which are advantageous in that a fertilized embryo is not required for their derivation, are amenable to molecular modifications that bring them functionally closer to true ES cells.