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

Autor: Ryuichi Ono, Kenji Nakamura, Kimiko Inoue, Mie Naruse, Takako Usami, Noriko Wakisaka-Saito, Toshiaki Hino, Suzuki-Migishima, Rika, Narumi Ogonuki, Hiromi Miki, Takashi Kohda, Atsuo Ogura, Minesuke Yokoyama, Tomoko Kaneko-Ishino, Fumitoshi Ishino
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Zdroj: Nature Genetics; Jan2006, Vol. 38 Issue 1, p101-106, 6p, 2 Color Photographs, 2 Black and White Photographs, 2 Diagrams, 1 Chart
Abstrakt: 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. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index