The non-viability of uniparental mouse conceptuses correlates with the loss of the products of imprinted genes.
Diploid parthenogenetic or androgenetic mouse conceptuses produce characteristic and opposite mutant phenotypes and are non-viable, presumably due to different contributions from the maternal and paternal genomes. 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 Igf2 and Snrpn and the maternal alleles of Igf2r and H19 are active, while their opposite parental alleles are inactive. Here we demonstrate that the expression patterns of the Igf2 and Igf2r genes in androgenetic and parthenogenetic conceptuses correlate with which parental alleles normally express them, implying that the imprint can be maintained in the absence of the other parent's genome for these genes. This also indicates that both types of uniparental conceptuses are lacking developmentally important gene products. We did find, however, that the H19 gene was highly expressed not only in the parthenogenetic conceptus, but also in giant trophoblasts and secondary giant cells in the androgenetic placenta, in spite of the imprinting of the H19 gene in normal mouse extra embryonic tissues. We discuss these observations with respect to the non-viability of uniparental conceptuses and the reciprocal imprinting patterns of the Igf2 and H19 genes.
Walsh
C
C
Institute for Experimental Drug Research, Karolinska Hospital, Stockholm, Sweden.
Glaser
A
A
Fundele
R
R
Ferguson-Smith
A
A
Barton
S
S
Surani
M A
MA
Ohlsson
R
R
D000818:Animals; D004247:DNA / Q000032:analysis / Q000235:genetics; D004622:Embryo, Mammalian / Q000502:physiology*; D005314:Embryonic and Fetal Development / Q000235:genetics*; D005260:Female; D015870:Gene Expression; D005796:Genes; D016678:Genome; D017403:In Situ Hybridization; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D009154:Mutation; D010312:Parthenogenesis / Q000502:physiology*; D010641:Phenotype; D014158:Transcription, Genetic
D004247:DNA