
pmid: 4396267
Abstract Polyoma and SV 40-transformed cells carry multiple copies of the entire genome in their chromosomes; the viral DNA sequences appear to be covalently integrated into the host cell’s DNA but it is not known whether they are clustered in a reiterated tandem sequence or whether they are distributed singly or in clusters throughout the cell’s chromosomes. Some of the viral genes are transcribed into RNA and may code for the virus-specific antigens found in transformed cells. 3T3 cells transformed with a thermosensitive mutant of polyoma (Ts-a) can be induced to produce virus if the cells (Ts-a-3T3) are transferred from 38.5 to 31 °C. The data suggest that induction of viral multiplication involves the asynchronous occurrence of a unique event, after which DNA synthesis can continue even under non-permissive conditions. Superhelical closed circular dimers and trimers of polyoma DNA are synthesized as well as monomeric molecules. These oligomers can amount to 40 % of the total viral DNA; they are not obligatory precursors of the monomeric form, which is the only type found in mature virions. Oligomers are only infrequently observed (1 % or less) after infection of 3T3 cells with either wild type of the Ts-a mutant of polyoma. Several possible models to explain the origin of oligomers, the state of viral DNA in transformed cells and the nature of the activating event are discussed.
DNA Replication, Simian virus 40, Virus Replication, Chromosomes, Cell Line, Cytogenetics, Mice, Microscopy, Electron, Cytopathogenic Effect, Viral, Culture Techniques, Histocompatibility, DNA, Viral, Mutation, Animals, RNA, Viral, Antigens, Polyomavirus
DNA Replication, Simian virus 40, Virus Replication, Chromosomes, Cell Line, Cytogenetics, Mice, Microscopy, Electron, Cytopathogenic Effect, Viral, Culture Techniques, Histocompatibility, DNA, Viral, Mutation, Animals, RNA, Viral, Antigens, Polyomavirus
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