Birth of parthenogenetic mice that can develop to adulthood

  title={Birth of parthenogenetic mice that can develop to adulthood},
  author={Tomohiro Kono and Yayoi Obata and Quiong Wu and Katsutoshi Niwa and Yukiko Ono and Yuji Yamamoto and Eun S Park and Jeong-Sun Seo and Hidehiko Ogawa},
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…

Genomic imprinting is a barrier to parthenogenesis in mammals

  • T. Kono
  • Biology
    Cytogenetic and Genome Research
  • 2006
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.

Birth of Parthenote Mice Directly from Parthenogenetic Embryonic Stem Cells

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.

Polyploidy of semi-cloned embryos generated from parthenogenetic haploid embryonic stem cells

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.

Functional full-term placentas formed from parthenogenetic embryos using serial nuclear transfer

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.

Birth of mice produced by germ cell nuclear transfer

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.

Three paternally imprinted regions are sequentially required in prenatal and postnatal mouse development

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.

Genetic modification for bimaternal embryo development.

  • T. Kono
  • Biology
    Reproduction, fertility, and development
  • 2009
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.

Regulated expression of two sets of paternally imprinted genes is necessary for mouse parthenogenetic development to term.

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.

Parthenogenetic Embryonic Stem Cells in Nonhuman Primates

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.

High-frequency generation of viable mice from engineered bi-maternal embryos

The results provide conclusive evidence that imprinted genes regulated by these two paternally methylated imprinting-control regions are the only paternal barrier that prevents the normal development of bi-maternal mouse fetuses to term.



Mouse parthenogenetic embryos with monoallelic H19 expression can develop to day 17.5 of gestation.

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.

Epigenetic modifications during oocyte growth correlates with extended parthenogenetic development in the mouse

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).

Development of reconstituted mouse eggs suggests imprinting of the genome during gametogenesis

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.

Maternal Primary Imprinting Is Established at a Specific Time for Each Gene throughout Oocyte Growth*

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.

Disruption of primary imprinting during oocyte growth leads to the modified expression of imprinted genes during embryogenesis.

The results show that primary imprinting during oocyte growth exhibits a crucial effect on both the expression and repression of maternal alleles during embryogenesis.

Genome imprinting and development in the mouse.

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.

Roles for genomic imprinting and the zygotic genome in placental development

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.

Mechanisms of genomic imprinting.

  • K. Pfeifer
  • Biology
    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 will

Development of gynogenetic eggs in the mouse: implications for parthenogenetic embryos.

Mouse eggs with different genetic constitutions prepared by micromanipulation of fertilized diploids and triploids developed at best to about the 25-somite stage as did the genetically similar diploid parthenogenones stimulated to develop in the complete absence of the male gamete.