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Recombination during early herpes simplex virus type 1 infection is mediated by cellular proteins.

Artikel i vetenskaplig tidskrift
Författare X D Yao
Per Elias
Publicerad i The Journal of biological chemistry
Volym 276
Nummer/häfte 4
Sidor 2905-13
ISSN 0021-9258
Publiceringsår 2001
Publicerad vid Institutionen för medicinsk och fysiologisk kemi
Sidor 2905-13
Språk en
Länkar dx.doi.org/10.1074/jbc.M005627200
Ämnesord 3T3 Cells, Animals, Cells, Cultured, Cricetinae, DNA Replication, DNA, Viral, metabolism, Herpesvirus 1, Human, genetics, Kidney, cytology, Mice, Plasmids, metabolism, Recombination, Genetic, Repetitive Sequences, Nucleic Acid, Sequence Homology, Nucleic Acid
Ämneskategorier Virologi, Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)

Sammanfattning

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.

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