Cell proliferation is reduced in parthenogenetic mouse embryos at the blastocyst stage: a quantitative study.
Parthenogenetic and androgenetic embryos fail to develop to term, possibly because of genomic imprinting, an epigenetic alteration of certain genes, depending on the parent of origin. The effect of this phenomenon has been studied mainly in mid-gestation embryos, without morphological abnormalities detected during the preim-plantation period. Nevertheless, parthenogenetic mouse embryos never develop to the blastocyst stage in the same numbers as do fertilized ones, and up to 50% fail to implant, suggesting that genomic imprinting may be responsible for this lack of viability.



We have made a quantitative and morphometric analysis of the cell proliferation capacity at the end of the preimplantation period in parthenogenetic mice to study if such parameter is affected by the monoparental constitution of the embryos.



We have found that, apart from the different morphology and cell number induced by culture conditions, parthenogenetic mouse blastocysts have a significantly smaller cell number than do fertilized control embryos. Our interpretation of these results is that the monoparental constitution of these embryos may be responsible for the lack of some factor required to sustain cell proliferation after the morula stage.
Uranga
J A
JA
Department of Cell Biology, University of the Basque Country Medical School, Leioa (Vizcaya), Spain.
Aréchaga
J
J
D000818:Animals; D001755:Blastocyst / Q000166:cytology*; D002455:Cell Division; D048429:Cell Size; D018392:Genomic Imprinting; D051379:Mice; D010312:Parthenogenesis