The Use of DNA Tumour Viruses as Model Systems for Studying Damage and Repair of Eukaryotic Chromosomes: Analysis of Mutations by DNA Sequencing
Attempts to define repair processes in eukaryotic systems are subject to all the difficulties inherent in studying very large and complex DNA molecules. When the location of a lesion that makes repair necessary for the efficient functioning of a cell cannot in itself be precisely defined, it is not surprising that the subsequent repair process can only be described in general terms, usually related to phenotypic responses. The idea that viruses might be used as probes for studying repair of DNA in mammalian cells has been put forward in a number of papers and a limited number of experiments have been carried out with this aim in mind. The conclusions from some of these studies, presented and summarised by Day (1978), do not make very encouraging reading. Nonetheless, it would seem premature to abandon the approach, particularly when one considers the remarkable advances made in the past few years in defining the molecular biology of some of the animal viruses and the promising efforts to correlate particular regions of viral genomes with biological activities inside the cell. For the purposes of this communication, I shall concentrate on the small DNA tumour viruses, the mouse virus, polyoma, the monkey virus, SV40, and the human variant of SV40, BKV as being among the better-characterised and most amenable to study of these viruses.
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