Abstract
Although both parental sexes contribute equivalent genetic information to the zygote, in mammals this information is not necessarily functionally equivalent. Diploid parthenotes possessing two maternal genomes are generally inviable1, embryos possessing two paternal genomes in man may form hydatidiform moles2, and nuclear transplantation experiments in mice have shown that both parental genomes are necessary for complete embryogenesis3–6. Not all of the genome is involved in these parental effects, however, because zygotes with maternal or paternal disomy for chromosomes 1, 4, 5, 9, 13, 14 and 15 of the mouse survive normally7,8. On the other hand, only the maternal X chromosome is active in mouse extraembryonic membranes9, maternal disomy 6 is lethal7, while non-complementation of maternal duplication/paternal deficiency or its reciprocal for regions of chromosome 2, 8 and 17 has been recognized10–12. We report that animals with maternal duplication/paternal deficiency and its reciprocal for each of two particular chromosome regions show anomalous phenotypes which depart from normal in opposite directions, suggesting a differential functioning of gene loci within these regions. A further example of non-complementation lethality is also reported.
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Cattanach, B., Kirk, M. Differential activity of maternally and paternally derived chromosome regions in mice. Nature 315, 496–498 (1985). https://doi.org/10.1038/315496a0
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DOI: https://doi.org/10.1038/315496a0
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