1. Department of BioScience, Tokyo University of Agriculture, Setagaya-ku, Tokyo 156-8502, Japan
2. Department of Applied Science, Tokyo University of Agriculture, Setagaya-ku, Tokyo 156-8502, Japan
3. Bio-oriented Technology Research Advancement Institution (BRAIN), Minato-ku, Tokyo 105-0001, Japan
4. MacroGen Inc, Chongno-Ku, Seoul 110-061, Korea
5. Department of Biochemistry, Seoul National University College of Medicine, Chongno-Ku, Seoul 110-799, Korea

Correspondence to: Tomohiro Kono^1,3 Email: tomohiro@nodai.ac.jp

Only mammals have relinquished parthenogenesis, a means of producing descendants solely from maternal germ cells. Mouse parthenogenetic embryos die by day 10 of gestation^{1, 2, 3, 4}. Bi-parental reproduction is necessary because of parent-specific epigenetic modification of the genome during gametogenesis^{5, 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.

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