DEFECTIVE CHORIOALLANTOIC FUSION IN MIDGESTATION LETHALITY OF PARTHENOGENONE[--]TETRAPLOID CHIMERAS

Previous studies of parthenogenetic embryos revealed severe perturbati ons of both embryonic and extraembryonic tissue lineages during postim plantation development. The majority of pure parthenogenetic concepti have no recognizable axis and exhibit preferential terminal differenti ation of their trophectoderm and primitive endoderm. To further define the role of the extraembryonic lineages in parthenogenetic developmen t, we provided them with zygote-derived extraembryonic tissues by aggr egating them with fertilized tetraploid embryos. On Day 12 of combined in vitro and in vivo development, most of the embryos proper in these chimeras were entirely derived parthenogenetically, whereas their tro phectoderm and primitive endoderm tissues were derived from the tetrap loid component. No Igf2 expression was detected in the parthenogenetic embryo proper, indicating that imprinting was manifested in such chim eras. Typical development of the parthenogenetic embryo proper was mar kedly improved in comparison with pure parthenogenetic concepti, with such chimeras attaining an average of 23 somites (range, 10 to 35). Ho wever, most of the chimeras died abruptly at Day 13, and all were bein g resorbed at Day 14 of development. The gross normality of axial stru ctures and organ development suggests that a major cause of failure of these chimeric parthenogenones to survive beyond mid-gestation was du e to defective chorioallantoic fusion. Our results indicate that the s evere perturbation of axial development seen in most pure parthenogene tic concepti is a secondary consequence of the effects of parthenogene sis on the trophectoderm and primitive endoderm lineages. Moreover, th e mid-gestation death of parthenogenetic embryos proper despite the pr esence of zygote-derived tetraploid tissues implicates extraembryonic mesoderm in manifesting the effects of genomic imprinting. (C) 1996 Ac ademic Press, Inc.