THE NON-VIABILITY OF UNIPARENTAL MOUSE CONCEPTUSES CORRELATES WITH THE LOSS OF THE PRODUCTS OF IMPRINTED GENES

Diploid parthenogenetic or androgenetic mouse conceptuses produce char acteristic and opposite mutant phenotypes and are non-viable, presumab ly due to different contributions from the maternal and paternal genom es. This is likely to be the result of the preferential expression of only one parent's copy of certain genes in the offspring. So far, four such endogenous imprinted genes are known: the paternal alleles of Ig f2 and Snrpn and the maternal alleles of Igf2r and H19 are active, whi le their opposite parental alleles are inactive. Here we demonstrate t hat the expression patterns of the Igf2 and Igf2r genes in androgeneti c and parthenogenetic conceptuses correlate with which parental allele s normally express them, implying that the imprint can be maintained i n the absence of the other parent's genome for these genes. This also indicates that both types of uniparental conceptuses are lacking devel opmentally important gene products. We did find, however, that the H19 gene was highly expressed not only in the parthenogenic conceptus, bu t also in giant trophoblasts and secondary giant cells in the androgen etic placenta, in spite of the imprinting of the H19 gene in normal mo use extra embryonic tissues. We discuss these observations with respec t to the non-viability of uniparental conceptuses and the reciprocal i mprinting patterns of the Igf2 and H19 genes.