Inviability of parthenogenones is determined by pronuclei, not egg cytoplasm

Abstract

Parthenogenetic mouse embryos pose an interesting problem in the study of early mammalian development. Haploid or diploid parthenogenones, resulting from spontaneous¹ or experimental^2–4 activation of unfertilized eggs, will undergo apparently normal preimplantation development but die in the early post-implantation stages^5–8. However, in aggregation chimaeras with fertilized embryos, parthenogenetic embryos have the ability to differentiate into many tissue types, including gametes which can give rise to normal offspring⁹. Furthermore, it has been reported that viable young were obtained from the transfer of inner cell-mass nuclei of parthenogenetic blastocysts to enucleated fertilized eggs¹⁰. These observations suggest that sperm have some additional role, apart from restoring a complete genome, that is necessary for normal development. To investigate whether sperm-related modifications to the egg cytoplasm are important, we have used an efficient nuclear transfer technique in which a complete karyoplast, comprised of pronuclei, surrounding cytoplasm and a portion of the egg plasma membrane, is transferred utilizing Sendai virus membrane fusion¹¹. Embryos produced by the transfer of pronuclei from diploid parthenogenetic eggs to enucleated fertilized eggs died very soon after implantation, whereas viable young were obtained from the transfer of fertilized egg pronuclei into enucleated parthenogenetic eggs. This shows that the death of parthenogenones is not due to a lack of cytoplasmic factors from the sperm.