Effects of Imprinting on Early Development of Mouse Embryos

During the past decade, a major advance in understanding the development of embryonic and extraembryonic lineages of mammals has emerged from studies on the fate of parthenogenetic (or gynogenetic) embryos and their androgenetic counterparts. Diploid parthenogenotes produced by experimentally activating mouse oocytes develop to midgestation stages, then they die with a characteristic phenotype: The most advanced embryos have extensive development of the axial embryonic structures (brain and neural tube, somites) and other embryonic organs, but only rudimentary development of the trophoblast lineage (1). Diploid androgenotes— that is, embryos with only paternally derived chromosomes—that are manufactured by nuclear transfer (2) also die at midgestation stages, but with retarded development of the embryo proper and with normal trophoblast by gross morphological examination (1, 3). The conclusion drawn from these and other studies (reviewed in 4–6) is that maternal and paternal gametes make distinct and complementary contributions to the developing conceptus, so that normal mouse development requires both maternal and paternal haploid genomes (1, 7). This phenomenon, referred to as genomic imprinting, thus appears to have profound consequences for peri-implantation development in eutherian mammals (metatheria and prototheria have not been studied).