The non-viability of uniparental mouse conceptuses correlates with the loss of the products of imprinted genes
The non-viability of uniparental mouse conceptuses correlates with the loss of the products of imprinted genes
复制标题
DOI:
10.1016/0925-4773(94)90037-x
复制
发表时间:
1994-04
影响因子:
2.6
通讯作者:
C. Walsh;A. Glaser;R. Fundele;A. Ferguson-Smith;S. Barton;M. Surani;R. Ohlsson
中科院分区:
文献类型:
--
作者:
C. Walsh;A. Glaser;R. Fundele;A. Ferguson-Smith;S. Barton;M. Surani;R. Ohlsson
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 ofIgf2andSnrpnand the maternal alleles ofIgf2randH19are active, while their opposite parental alleles are inactive. Here we demonstrate that the expression patterns of theIgf2andIgf2rgenes 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 theH19gene 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 theH19gene 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 theIgf2andH19genes.