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J. Biol. Chem., Vol. 276, Issue 4, 2905-2913, January 26, 2001
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From the Homologous recombination was examined in cells
infected with herpes simplex virus type I. Circular and linear DNA with
directly repeated sequences was introduced as recombination substrates into cells. Recombination was measured either by
origin-dependent amplification of recombination products or
by recombination-dependent expression of luciferase from a
disrupted gene. Homologous recombination in baby hamster kidney
cells converted linear DNA to circular templates for DNA replication
and luciferase expression in the complete absence of virus. The
products of homologous recombination were efficiently amplified by the
viral replication apparatus. The efficiency of recombination was
dependent on the structure of the substrate as well as the cell type.
Linear DNA with the direct repeats at internal positions failed to
recombine in Balb/c 3T3 cells and induced p53-dependent
apoptosis. In contrast, linear DNA with directly repeated sequences
precisely at the ends recombined and replicated in 3T3 cells.
Homologous recombination in baby hamster kidney cells did not depend on
the position of the repeated sequences. We conclude that homologous
recombination is independent of viral gene functions and that it is
likely to be carried out by cellular proteins. We suggest that
homologous recombination between directly repeated sequences in the
linear herpes simplex virus type 1 chromosome may help to avoid
p53-dependent apoptosis and to promote viral DNA replication.
Recombination during Early Herpes Simplex Virus Type 1 Infection
Is Mediated by Cellular Proteins*
and Department of Molecular Biology and
Genetics, College of Biological Science, University of Guelph, Guelph,
Ontario N1G 2W1, Canada and the § Department of Medical
Biochemistry, Göteborg University, Box 440, Göteborg SE 405 30, Sweden
*
This work was supported by Medical Research Council Grant
K99-31X-12199-03C and Swedish Cancer Society Grant 2552-B97-11XAC.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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