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

Qiong Wu, Takuya Kumagai, Manabu Kawahara, Hidehiko Ogawa, Hitoshi Hiura, Yayoi Obata, Riya Takano, Tomohiro Kono

Research output: Contribution to journalArticlepeer-review

38 Citations (Scopus)

Abstract

Mouse parthenogenetic embryos (PEs) are developmentally arrested until embryo day (E) 9.5 because of genomic imprinting. However, we have shown that embryos containing genomes from non-growing (ng) and fully grown (fg) oocytes, i.e. ngwt/fgwt PE (wt, wild type), developed to E13.5. Moreover, parthenogenetic development could be extended to term by further regulation of Igf2 and H19 expression using mice with deletion of the H19 transcription unit (H19Δ13) together with its differentially unit (DMR). To gain an insight into the extended development of the parthenotes to term, we have here investigated the expression levels of paternally imprinted genes in ngH19Δ13/fgwt PE throughout their development. In ngH19Δ13/fgwt Pes that died soon after recovery, the expression of Igf2 and H19 was restored to the appropriate levels except for low Igf2 expression in the liver after E15.5. Further, the paternally expressed Dlk1 and Dio3 were repressed, while the expression levels of the maternal Gtl2 and Mirg were twice those of the controls. However, the above-mentioned four genes showed almost normal expression in the surviving ngH19Δ13/fgwt PEs. The methylation analysis revealed that the intragenic DMR of the Dlk1-Gtl2 domain was hypermethylated in the ngH19Δ13/fgwt PEs that survived, but not in the PEs that died soon after recovery. 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.

Original languageEnglish
Pages (from-to)481-488
Number of pages8
JournalReproduction
Volume131
Issue number3
DOIs
Publication statusPublished - 2006 Mar

ASJC Scopus subject areas

  • Reproductive Medicine
  • Embryology
  • Endocrinology
  • Obstetrics and Gynaecology
  • Cell Biology

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