Article

Deletion of Peg10, an imprinted gene acquired from a retrotransposon, causes early embryonic lethality.

Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kandasurugadai, Chiyoda-ku, Tokyo 101-0062, Japan.
Nature Genetics (impact factor: 35.53). 02/2006; 38(1):101-6. DOI:10.1038/ng1699 pp.101-6
Source: PubMed

ABSTRACT By comparing mammalian genomes, we and others have identified actively transcribed Ty3/gypsy retrotransposon-derived genes with highly conserved DNA sequences and insertion sites. To elucidate the functions of evolutionarily conserved retrotransposon-derived genes in mammalian development, we produced mice that lack one of these genes, Peg10 (paternally expressed 10), which is a paternally expressed imprinted gene on mouse proximal chromosome 6. The Peg10 knockout mice showed early embryonic lethality owing to defects in the placenta. This 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.

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Keywords

elucidate
 
embryonic lethality
 
evolutionarily conserved retrotransposon-derived gene
 
evolutionarily conserved retrotransposon-derived genes
 
first direct evidence
 
imprinted gene
 
mammalian genomes
 
mouse parthenogenetic development
 
mouse proximal chromosome 6
 
Peg10 knockout mice
 
transcribed Ty3/gypsy retrotransposon-derived genes