Erasing genomic imprinting memory in mouse clone embryos produced from day 11.5 primordial germ cells.
Analysis of parental-origin-specific expression of imprinted genes and DNA methylation patterns of differentially methylated regions in embryos and clones derived from both male and female PGCs provides strong evidence that the erasure process of genomic imprinting memory proceeds in the day 10.5 to day 11.5 PGC.
Peg1/Mest imprinted gene on chromosome 6 identified by cDNA subtraction hybridization
Peg1 (paternally expressed gene 1) or Mest, the first imprinted gene found on the mouse chromosome 6, may contribute to the lethality of parthenogenones and of embryos with a maternal duplication for the proximal chromosome 6.
Deletion of Peg10, an imprinted gene acquired from a retrotransposon, causes early embryonic lethality
The production of mice that lack Peg10 indicates that Peg10 is critical for mouse parthenogenetic development and provides the first direct evidence of an essential role of an evolutionarily conserved retrotransposon-derived gene in mammalian development.
Identification of an imprinted gene, Meg3/Gtl2 and its human homologue MEG3, first mapped on mouse distal chromosome 12 and human chromosome 14q
For the isolation of imprinted genes in this region, a systematic screen of maternally expressed genes (Megs) was carried out by the subtraction‐hybridization method using androgenetic and normally fertilized embryos.
Identification of a large novel imprinted gene cluster on mouse proximal chromosome 6.
- R. Ono, Hirosuke Shiura, H. Aburatani, T. Kohda, T. Kaneko-Ishino, F. Ishino
- BiologyGenome Research
- 1 July 2003
A differentially methylated region established in sperm and eggs is located just within the region containing the two first exons of Peg10 and Sgce, and may play an important role in regulating the two paternally expressed genes: Peg 10 and SGce.
Role of retrotransposon-derived imprinted gene, Rtl1, in the feto-maternal interface of mouse placenta
It is demonstrated that retrotransposon-derived Rtl1 (retrotranspos on-like 1), also known as Peg11 (paternally expressed 11), is essential for maintenance of the fetal capillaries, and that both its loss and its overproduction cause late-fetal and/or neonatal lethality in mice.
Imprinting regulation of the murine Meg1/Grb10 and human GRB10 genes; roles of brain-specific promoters and mouse-specific CTCF-binding sites.
The insulator function of CTCF might cause reciprocal maternal expression of the Meg1/Grb10 gene from another upstream promoter in the mouse, whereas the human upstream promoter is active in both parental alleles due to the lack of the corresponding insulator sequence in this region.
A retrotransposon-derived gene, PEG10, is a novel imprinted gene located on human chromosome 7q21.
Analysis of two predicted open reading frames revealed that ORF1 and ORF2 have homology to the gag and pol proteins of some vertebrate retrotransposons, respectively, which suggest that PEG10 is derived from a retro transposon that was previously integrated into the mammalian genome.
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.
Peg3 imprinted gene on proximal chromosome 7 encodes for a zinc finger protein
It is found that maternal duplication of the proximal chromosome 7 causes neonatal lethality and this region is syntenic with human chromosome 19q13.3 (refs 10,11), where the genes for myotonic dystrophy and a putative tumour suppressor gene are located12,13.