Human Molecular Genetics, Vol 6, 325-332, Copyright © 1997 by Oxford University Press
R Wevrick and U Francke
The Prader-Willi syndrome (PWS) is caused by genomic alterations that
inactivate imprinted, paternally expressed genes in human chromosome region
15q11-q13. IPW, a paternally expressed gene cloned from this region, is not
expressed in individuals with PWS, and is thus a candidate for involvement
in this disorder. The IPW transcript does not appear to encode a
polypeptide, suggesting that it functions at the level of an RNA. We have
now cloned a mouse gene, named Ipw, that has sequence similarity to a part
of IPW and is located in the conserved homologous region of mouse
chromosome 7. The Ipw cDNA also contains no long open reading frame, is
alternatively spliced and contains multiple copies of a 147 bp repeat,
arranged in a head-to-tail orientation, that are interrupted by the
insertion of an intracisternal A particle sequence. Ipw is expressed
predominantly in brain. In an interspecies (M.musculus x M.m.castaneus) F1
hybrid animal, expression of Ipw is limited to the paternal allele. We
propose that Ipw is the murine homolog of IPW.
ARTICLES
An imprinted mouse transcript homologous to the human imprinted in Prader-Willi syndrome (IPW) gene
Department of Genetics, Stanford University School of Medicine, CA 94305-5428, USA.
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