Defective Chorioallantoic Fusion in Mid-gestation Lethality of Parthenogenone ⇔ Tetraploid Chimeras

Abstract

Previous studies of parthenogenetic embryos revealed severe perturbations of both embryonic and extraembryonic tissue lineages during postimplantation development. The majority of pure parthenogenetic concepti have no recognizable axis and exhibit preferential terminal differentiation of their trophectoderm and primitive endoderm. To further define the role of the extraembryonic lineages in parthenogenetic development, we provided them with zygote-derived extraembryonic tissues by aggregating 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 trophectoderm and primitive endoderm tissues were derived from the tetraploid component. No Igf2 expression was detected in the parthenogenetic embryo proper, indicating that imprinting was manifested in such chimeras. Typical development of the parthenogenetic embryo proper was markedly improved in comparison with pure parthenogenetic concepti, with such chimeras attaining an average of 23 somites (range, 10 to 35). However, most of the chimeras died abruptly at Day 13, and all were being resorbed at Day 14 of development. The gross normality of axial structures and organ development suggests that a major cause of failure of these chimeric parthenogenones to survive beyond mid-gestation was due to defective chorioallantoic fusion. Our results indicate that the severe perturbation of axial development seen in most pure parthenogenetic concepti is a secondary consequence of the effects of parthenogenesis on the trophectoderm and primitive endoderm lineages. Moreover, the mid-gestation death of parthenogenetic embryos proper despite the presence of zygote-derived tetraploid tissues implicates extraembryonic mesoderm in manifesting the effects of genomic imprinting.

Structural chromosomal abnormalities in couples with recurrent abortion in Egypt

“…Sperm quality is often associated with the embryo's ability to progress to implantation. Paternally expressed genes modulate the proliferation and invasiveness of trophoblast cells and subsequent placental proliferation (29,30). Furthermore, evidence suggests that abnormalities in sperm DNA may affect embryo development and possibly increase the risk of miscarriage (31).…”

Xist-deficient mice are defective in dosage compensation but not spermatogenesis.

“…2E) and frequently included a balloon-like structure protruding from the caudal end of the embryo, probably the allantois (Fig. 2E) (Spindle et al 1996). A subset of the E8.5 mutant embryos had developed further, and specific tissues and structures could be identified.…”

Functional full-term placentas formed from parthenogenetic embryos using serial nuclear transfer

“…In the chimera method, parthenogenetic embryos or pES cells were aggregated with fertilised tetraploid embryos to introduce a normal placenta derived from a wild-type embryo and most of them failed to develop to full term (Barton et al, 1985;Chen et al, 2009;Spindle et al, 1996;Thomson and Solter, 1988). Therefore, it was concluded that differences in cell origin between foetus and placenta could not support foetal development effectively.…”