Premium
Disruption of the genomic imprint in trans with homologous recombination at Snrpn in ES cells
Author(s) -
Tsai TingFen,
Bressler Jan,
Jiang Yonghui,
Beaudet Arthur L.
Publication year - 2003
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/gene.10237
Subject(s) - homologous recombination , genetics , homologous chromosome , biology , recombination , gene
Summary: In gene targeting studies of the Prader‐Willi syndrome (PWS)/Angelman syndrome (AS) domain in mouse ES cells, we recovered only recombinants with the paternal allele for constructs at exons 2 or 3 of the imprinted, maternally silenced Snurf‐Snrpn gene. These sites lie close to the imprinting center (IC) for this domain. In contrast, recombinants for Ube3a within the same imprinted domain were recovered with equal frequency on the maternal and paternal alleles. In addition, gene targeting of the paternal allele for Snurf‐Snrpn resulted in partial or complete demethylation in trans with activation of expression for the previously silenced maternal allele. The imprint switching of the maternal allele in trans is not readily explained by competition for trans ‐acting factors and adds to a growing body of evidence indicating homologous association of oppositely imprinted chromatin domains in somatic mammalian cells. genesis 37:151–161, 2003. © 2003 Wiley‐Liss, Inc.