Human Molecular Genetics, Vol 7, 91-95, Copyright © 1998 by Oxford University Press
JM Greally, DJ Starr, S Hwang, L Song, M Jaarola and S Zemel
Genes subject to genomic imprinting generally occur in clusters of hundreds
of kilobases. These domains exhibit several gamete of origin- dependent
manifestations, including a pattern of asynchronous replication when
studied by fluorescence in situ hybridization (FISH). We find a transition
from asynchronous replication at the imprinted mouse H19 gene to
synchronous replication at the downstream Rpl23 gene, the human homologue
of which appears to be non-imprinted. Two-colour FISH demonstrates that
this transition is due solely to a difference in replication timing between
the upstream and downstream chromatin on the later-replicating (maternal)
chromosome. This difference is lost in mice deleted for the H19 gene body
and 9.9 kb of upstream DNA when this deletion is maternally inherited, with
synchronous replication patterns extending over 110 kb upstream from the
deleted area. No effect is seen when the deletion is paternally inherited.
The presence of a boundary element in this region has been suggested by
observations of position- independent expression of H19 -containing
transgenes and the blocking of accessibility of downstream enhancers to the
upstream Igf2 and Ins2 genes on the maternal chromosome. The FISH studies
presented here demonstrate the insulation of replication patterns within
the imprinted domain from downstream, non-imprinted chromatin, mediated by
an element at the H19 locus which is subject to genomic imprinting.
ARTICLES
The mouse H19 locus mediates a transition between imprinted and non- imprinted DNA replication patterns
Department of Genetics, Yale University School of Medicine, 333 Cedar Street, PO Box 208081, New Haven, CT 06520-8081, USA.
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