Impaired gene activity for 18S and 28S rRNA in early embryonic development of mouse parthenogenones

ALTHOUGH many unfertilised mouse oocytes have been variously stimulated to develop into embryos—parthenogenones—all have died soon after implantation1. The suggested causes of this failure include homozygosity of recessive lethals and an incomplete cortical reaction1. It is not known whether the lack of the paternally-derived genome inhibits their proper development. Using selective silver staining2,3 we have examined the activity of the genes for 18S and 28S ribosomal RNA during preimplantation development of parthenogenones. From studies of the activity of nucleolus organisers on the chromosomes of human–mouse cell hybrids, it has been assumed that silver precipitation was a consequence of gene activity for 18S and 28S rRNA (refs 4–6). Our results indicate that these genes are activated during early embryogenesis and without the need for paternally-derived factors.