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Parthenogenetic and androgenetic embryos do not reach term due to the process of genomic imprinting, an epigenetic modification of the DNA that results in parental-specific gene expression (Fundele and Surani, 1994). This phenomenon is being widely analysed by using embryonic stem cells (ES cells) derived from the epiblast of blastocysts at the time when such genome modification is supposed to occur. The restricted distribution of parthenogenetic and androgenetic ES cells in tissues has been studied in chimeras with normal host cells and in teratomas formed by ectopic transfer (Mann et a1., 1990; Allen et a1., 1994). However, considering the dynamic nature of epigenetic changes during early development and the instability of imprinting in ES cells, it is particularly interesting to examine their earlier differentiation pathways. We analysed parthenogenetic (PK1), androgenetic (AK1) and biparentat (AB1) cells W1tha senes of differentiation markers before and after induction of differentiation in vitro by culturing them in a medium without Leukemia Inhibitory Factor (lIF). Markers used were: alkaline phosphatase (AP) and anti-SSEA-1 for undifferentiated cells (Johnson et af., 1977; Fox et al., 1981), anti-SSEA-1 and TROMA antibody (anti-cytokeratin 8; Kemler et al., 1981) for differentiation to visceral endodenm, TROMA and anti-vimentin for parietal endodenmal (Lehtonen et 81 .,1983) and anti-vimentin for mesodermal cells (Franke et al., 1982).

Changes in the early differentiation pathway of monoparental embryonic stem cells is not affected by the expression of LIF receptors.