Disparate Replication Properties of Integrated and Extrachromosomal Forms of Bovine Papilloma Virus in ID13 Cells

Bovine papillomavirus (BPV) previously has been reported to exist in transformed rodent cell lines as both chromosomally integrated and extrachromosomal forms. In the BPV-transformed mouse cell line ID13, extrachromosomal BPV molecules replicate throughout S phase of the cell cycle in a random choic...

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Bibliographic Details
Published in:Journal of molecular biology 1995-11, Vol.254 (2), p.119-129
Main Authors: Ten Hagen, Kelly G., Ravnan, Julie-Britt, Cohen, Stanley N.
Format: Article
Language:English
Subjects:
Animals
Blotting, Southern
Bovine papillomavirus
Bovine papillomavirus 1 - genetics
Bovine papillomavirus 1 - physiology
BPV
Cattle
Cell Cycle
cell division
Cell Line, Transformed
cell lines
Cell Transformation, Viral
Centrifugation, Density Gradient
chromosomal insertion
chromosomes
Chromosomes - genetics
Clone Cells
Demecolcine - pharmacology
DNA
DNA Probes
DNA Replication
Electrophoresis, Gel, Pulsed-Field
extrachromosomal dna
Flow Cytometry
genome
In Situ Hybridization, Fluorescence
integrated dna
integration
Mice
replication
replication origin
S phase
timing of replication
transformation
Virus Integration
Virus Replication
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Description
Summary:Bovine papillomavirus (BPV) previously has been reported to exist in transformed rodent cell lines as both chromosomally integrated and extrachromosomal forms. In the BPV-transformed mouse cell line ID13, extrachromosomal BPV molecules replicate throughout S phase of the cell cycle in a random choice mode. We report here that these replication properties were altered for chromosomally integrated BPV DNA in five independent ID13 subclones. In all of the subclones, the integrated BPV sequences, which had no detectable deletions or mutations, existed in head-to-tail tandem arrays that replicated once per cell cycle, predomi nantly late in S phase. In contrast, extrachromosomal BPV molecules present in other subclones of the same cell line replicated in the random choice mode observed previously for non-integrated BPV. Our results indicate that the replication origin of integrated BPV either is inactivated as a consequence of chromosomal insertion, leading to the replication of BPV from origins in the flanking chromosomal DNA, or alternatively is reprogrammed to function in a once-per-cell cycle mode predominantly late in S phase.
ISSN:0022-2836
1089-8638
DOI:10.1006/jmbi.1995.0605