Birth of parthenogenetic mice that can develop to adulthood

Tomohiro Kono (), Yayoi Obata, Quiong Wu, Katsutoshi Niwa, Yukiko Ono, Yuji Yamamoto, Eun Sung Park, Jeong-Sun Seo and Hidehiko Ogawa
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Tomohiro Kono: Tokyo University of Agriculture
Yayoi Obata: Tokyo University of Agriculture
Quiong Wu: Tokyo University of Agriculture
Katsutoshi Niwa: Tokyo University of Agriculture
Yukiko Ono: Tokyo University of Agriculture
Yuji Yamamoto: Tokyo University of Agriculture
Eun Sung Park: MacroGen Inc
Jeong-Sun Seo: MacroGen Inc
Hidehiko Ogawa: Tokyo University of Agriculture

Nature, 2004, vol. 428, issue 6985, 860-864

Abstract: Abstract Only mammals have relinquished parthenogenesis, a means of producing descendants solely from maternal germ cells. Mouse parthenogenetic embryos die by day 10 of gestation1,2,3,4. Bi-parental reproduction is necessary because of parent-specific epigenetic modification of the genome during gametogenesis5,6,7,8. This leads to unequal expression of imprinted genes from the maternal and paternal alleles9. However, there is no direct evidence that genomic imprinting is the only barrier to parthenogenetic development. Here we show the development of a viable parthenogenetic mouse individual from a reconstructed oocyte containing two haploid sets of maternal genome, derived from non-growing and fully grown oocytes. This development was made possible by the appropriate expression of the Igf2 and H19 genes with other imprinted genes, using mutant mice with a 13-kilobase deletion in the H19 gene10 as non-growing oocytes donors. This full-term development is associated with a marked reduction in aberrantly expressed genes. The parthenote developed to adulthood with the ability to reproduce offspring. These results suggest that paternal imprinting prevents parthenogenesis, ensuring that the paternal contribution is obligatory for the descendant.

Date: 2004
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DOI: 10.1038/nature02402

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