Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
2010-8-11
pubmed:abstractText
Mammalian parthenogenetic embryos invariably die in mid-gestation from imprinted gene defects and placental hypoplasia. Based on chimera experiments, trophoblastic proliferation is supposed to be inhibited in the absence of a male genome. Here, we show that parthenogenetic mouse embryonic cell nuclei can be reprogrammed by serial rounds of nuclear transfer without using any genetic modification. The durations of survival in uteri of cloned foetuses derived from green fluorescent protein (GFP)-labelled parthenogenetic cell nuclei were extended with repeated nuclear transfers. After five repeats, live cloned foetuses were obtained up to day 14.5 of gestation; however, they did not survive longer even when we repeated nuclear transfer up to nine times. All foetuses showed intestinal herniation and possessed well-expanded large placentas. When embryonic stem (ES) cells derived from fertilised embryos were aggregated with the cloned embryos, full-term offspring with large placentas were obtained from the chimeric embryos. Those placentas were derived from parthenogenetic cell nuclei, judging from GFP expression. The patterns of imprinted gene expression and methylation status were similar to their parthenogenetic origin, except for Peg10, which showed the same level as in the normal placenta. These 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1477-9129
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
137
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2841-7
pubmed:meshHeading
pubmed-meshheading:20659973-Animals, pubmed-meshheading:20659973-Base Sequence, pubmed-meshheading:20659973-Cell Differentiation, pubmed-meshheading:20659973-Cell Line, pubmed-meshheading:20659973-Cloning, Organism, pubmed-meshheading:20659973-DNA Methylation, pubmed-meshheading:20659973-DNA Primers, pubmed-meshheading:20659973-Embryonic Development, pubmed-meshheading:20659973-Embryonic Stem Cells, pubmed-meshheading:20659973-Female, pubmed-meshheading:20659973-Gene Expression, pubmed-meshheading:20659973-Genomic Imprinting, pubmed-meshheading:20659973-Male, pubmed-meshheading:20659973-Mice, pubmed-meshheading:20659973-Mice, Inbred C57BL, pubmed-meshheading:20659973-Mice, Inbred DBA, pubmed-meshheading:20659973-Mice, Inbred ICR, pubmed-meshheading:20659973-Mice, Transgenic, pubmed-meshheading:20659973-Nuclear Reprogramming, pubmed-meshheading:20659973-Nuclear Transfer Techniques, pubmed-meshheading:20659973-Parthenogenesis, pubmed-meshheading:20659973-Placenta, pubmed-meshheading:20659973-Pluripotent Stem Cells, pubmed-meshheading:20659973-Pregnancy, pubmed-meshheading:20659973-Totipotent Stem Cells, pubmed-meshheading:20659973-Transplantation Chimera
pubmed:year
2010
pubmed:articleTitle
Functional full-term placentas formed from parthenogenetic embryos using serial nuclear transfer.
pubmed:affiliation
RIKEN Center for Developmental Biology, Minatojima-minamimachi Chuo-ku, Kobe, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't