Development of gynogenetic and parthenogenetic inner cell mass and trophectoderm tissues in reconstituted blastocysts in the mouse
- PMID: 3834032
Development of gynogenetic and parthenogenetic inner cell mass and trophectoderm tissues in reconstituted blastocysts in the mouse
Abstract
The developmental potential of inner cell mass (ICM) and trophectoderm (TE) derived from parthenogenetic or biparental gynogenetic embryos was examined in reconstituted blastocysts with normal TE or ICM, respectively. The results demonstrate that when a normal ICM was introduced inside a trophectoderm vesicle derived from parthenogenetic or gynogenetic blastocysts, postimplantation development was characterized by the almost complete failure of trophoblast proliferation and without compensating cellular contribution from the normal ICM to the outer trophoblast lineage. Consequently, the normal ICMs also failed to develop adequately and only a few retarded embryos were detected on day 11-12 of pregnancy. In most respects, development of these reconstituted blastocysts resembled that obtained with unoperated gynogenetic and a parthenogenetic blastocyst. By contrast, an ICM from a parthenogenetic or gynogenetic embryo introduced inside a normal trophectoderm vesicle induced substantial proliferation of the trophoblast but again without a detectable cellular contribution from the ICM to the outer trophoblast lineage. However, with the improved development of the trophoblast, both the parthenogenetic and gynogenetic ICMs developed substantially better and without a detectable cellular contribution from the TE to the embryo. Almost all the embryos developed at least up to the 25-somite stage and many of them reached the 30- to 40-somite stage. Some of the most advanced day-11 and -12 gynogenones and parthenogenones yet seen have now been obtained in this way. Nevertheless, all the embryos were still smaller than the equivalent control embryos and showed signs of some tissue degeneration. The yolk sac was also suboptimal with poor blood supply and may need to be improved to obtain further improvement in the development of the embryos. The combined results demonstrate that the trophoblast proliferates very poorly even in the presence of a normal ICM, if the TE tissue lacks a paternal genome. However, ICM tissues which lack a paternal genome can develop to an advanced embryonic stage if they are introduced inside a normal trophectoderm vesicle. The results give further insight into the differential roles of maternal and paternal genomes during development of the embryo and extraembryonic tissues in the mouse.
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