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

First Author  Ono R Year  2006
Journal  Nat Genet Volume  38
Issue  1 Pages  101-6
PubMed ID  16341224 Mgi Jnum  J:106134
Mgi Id  MGI:3617664 Doi  10.1038/ng1699
Citation  Ono R, et al. (2006) Deletion of Peg10, an imprinted gene acquired from a retrotransposon, causes early embryonic lethality. Nat Genet 38(1):101-6
abstractText  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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