Birth of parthenogenetic mice that can develop to adulthood

@article{Kono2004BirthOP,
  title={Birth of parthenogenetic mice that can develop to adulthood},
  author={T. Kono and Y. Obata and Quiong Wu and K. Niwa and Y. Ono and Yuji Yamamoto and Eun S Park and Jeong-Sun Seo and H. Ogawa},
  journal={Nature},
  year={2004},
  volume={428},
  pages={860-864}
}
Only mammals have relinquished parthenogenesis, a means of producing descendants solely from maternal germ cells. [...] Key Method 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 gene 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…Expand
Genomic imprinting is a barrier to parthenogenesis in mammals
  • T. Kono
  • Medicine, Biology
  • Cytogenetic and Genome Research
  • 2006
TLDR
It is shown that alteration of maternal imprinting by oocyte reconstruction using non-growing oocytes, together with deletion of the H19 gene provide appropriate expression of imprinted genes from the maternal genome. Expand
Birth of Parthenote Mice Directly from Parthenogenetic Embryonic Stem Cells
TLDR
This study finds that derivation of pESCs is more efficient than of ESCs derived from fertilized embryos, in association with reduced mitogen‐activated protein kinase signaling in parthenogenetic embryos and their inner cell mass outgrowth, and shows that live parthenote pups were produced through tetraploid embryo complementation, which contributes to placenta development. Expand
Polyploidy of semi-cloned embryos generated from parthenogenetic haploid embryonic stem cells
TLDR
The generation of fertile semi-cloned mice is shown by injection of parthenogenetic haESCs (phaESCs) into oocytes after deletion of two differentially methylated regions (DMRs), the IG-D MR and H19-DMR. Expand
Polyploidy of semi-cloned embryos generated from parthenogenetic haploid embryonic stem cells
TLDR
The generation of fertile semi-cloned mice is shown by injection of parthenogenetic haESCs (phaESCs) into oocytes after deletions of two differentially methylated regions (DMRs), the IG-D MR and H19-DMR. Expand
Functional full-term placentas formed from parthenogenetic embryos using serial nuclear transfer
TLDR
The results suggest that there is a limitation for foetal development in the ability to reprogramme imprinted genes by repeated rounds of nuclear transfer, however, the placentas of parthenogenetic embryos can escape epigenetic regulation when developed using nuclear transfer techniques and can support foetAL development to full gestation. Expand
Birth of mice produced by germ cell nuclear transfer
TLDR
DNA methylation analyses showed that only embryos exhibiting normal imprinting developed to term, and germ cell differentiation is not an insurmountable barrier to cloning, and imprinting status is more important than the origin of the nucleus donor cell per se as a determinant of developmental plasticity following nuclear transfer. Expand
Three paternally imprinted regions are sequentially required in prenatal and postnatal mouse development
TLDR
Consistent with the essential functions of genomic imprinting in mammalian development, loss-of-function mouse genetic studies demonstrated that a portion of the imprinted genes such as Igf2 were essential for the survival of mouse embryos when they had been knocked out. Expand
Genetic modification for bimaternal embryo development.
  • T. Kono
  • Biology, Medicine
  • Reproduction, fertility, and development
  • 2009
TLDR
Using bimaternal embryos with two sets of maternal genomes, the present paper illustrates how parental methylation imprints are an obstacle to the progression of parthenogenesis. Expand
Regulated expression of two sets of paternally imprinted genes is necessary for mouse parthenogenetic development to term.
TLDR
The present study suggests that two sets of co-ordinately regulated but oppositely expressed genes, Igf2-H19 and Dlk1-Gtl2, act as a critical barrier to parthenogenetic development in order to render a paternal contribution obligatory for descendants in mammals. Expand
Parthenogenetic Embryonic Stem Cells in Nonhuman Primates
TLDR
PGES cells from nonhuman primate and human parthenogenetically activated oocyte have recently been derived and offer a valuable tool for studying the developmental, differentiation, and functional potential of the PGES cells in the context of their clinical application in organ and tissue transplantations in humans. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 36 REFERENCES
Mouse parthenogenetic embryos with monoallelic H19 expression can develop to day 17.5 of gestation.
TLDR
The present results suggest that the cessation of H19 gene expression from the ng-allele causes extended development of the fetus and that functional defects in the placenta could be fatal for the ontogeny. Expand
Epigenetic modifications during oocyte growth correlates with extended parthenogenetic development in the mouse
TLDR
The embryonic phenotypes observed here correlate with changes in epigenetic events that normally occur during oocyte growth, particularly the maternally expressed insulin-like growth factor II receptor gene (lgf2r). Expand
Development of reconstituted mouse eggs suggests imprinting of the genome during gametogenesis
TLDR
It is reported here that the eggs which receive a male pronucleus develop to term but those with two female pronuclei develop only poorly after implantation, suggesting that the cytoplasm of activated eggs is fully competent to support development toterm but not if the genome is entirely of maternal origin. Expand
Maternal Primary Imprinting Is Established at a Specific Time for Each Gene throughout Oocyte Growth*
TLDR
The results showed that the imprinting signals for each gene were not all imposed together at a specific time during oocyte growth but rather occurred throughout the period from primary to antral follicle stage oocytes. Expand
Disruption of primary imprinting during oocyte growth leads to the modified expression of imprinted genes during embryogenesis.
TLDR
The results show that primary imprinting during oocyte growth exhibits a crucial effect on both the expression and repression of maternal alleles during embryogenesis. Expand
Genome imprinting and development in the mouse.
TLDR
The cumulative effects of all the imprinted genes are observed in androgenones (AG) and parthenogenones (PG), which reveal complementary phenotypes with respect to embryonic and extraembryonic tissues. Expand
Roles for genomic imprinting and the zygotic genome in placental development
TLDR
It is shown that the spatial interactions between different cell types within feto-maternal interfaces are defective and abnormal behaviors in both zygote-derived and maternal cells that are attributed to the genome of theZygote but not the mother are identified. Expand
Parental origin-specific developmental defects in mice with uniparental disomy for chromosome 12.
TLDR
Ind imprinted genes on chromosome 12 are essential for viability, the regulation of prenatal growth, and the development of mesodermal and neural crest-derived lineages in mice. Expand
Completion of mouse embryogenesis requires both the maternal and paternal genomes
TLDR
It is concluded that the maternal and paternal contributions to the embryonic genome in mammals are not equivalent and that a diploid genome derived from only one of the two parental sexes is incapable of supporting complete embryogenesis. Expand
Mechanisms of genomic imprinting.
  • K. Pfeifer
  • Biology, Medicine
  • American journal of human genetics
  • 2000
Imprinted genes represent a curious defiance of normal Mendelian genetics. Mammals inherit two complete sets of chromosomes, one from the mother and one from the father, and most autosomal genes willExpand
...
1
2
3
4
...