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Extracellularly UV-damaged DNA induces mutations in intact parvovirus H-1 infecting mammalian cells
240 aliphatic fraction had no effect, with or without activation; the aromatic fraction showed the greatest mutagenicity with and without activation; the polar fraction was also mutagenic, but its metabolic activation did not enhance the effect. The active compounds in this last fraction could be represented, in significant part, by oxygenated derivatives of polycyclic aromatic hydrocarbons.
6 C. Dinsart, Z. Su, J. Cornelis and J. Rommelaere, Laboratoire de Biophysique et Radiobiologie, Universit~ Libre de Bruxelles, rue des Chevaux, 67, B-1640 RhodeSt-Gen~se
Extracellularly UV-damaged DNA induces mutations in intact parvovirus H-I infecting mammalian cells The frequency of mutants among the progeny of intact parvovirus H-1 is increased when cells are exposed to low doses of UV radiation or chemicals before virus infection. The same phenomenon is observed if cells are pretreated with UV-killed Simian virus 40 (SV40) or H-1 [1]. In a study on the nature of the signal that triggers the enhancement of viral mutagenesis, extracellularly UV-irradiated heterologous DNA from calf thymus or SV40 origin was introduced (by transfection) into undamaged human or rat cells before infection with a thermosensitive H-1 mutant. An enhanced number of wild-type virus revertants was produced in cells pretreated with UV-irradiated DNA as compared with controls infected with unirradiated DNA. About 2-fold increases in mutation frequency were observed; similar levels of mutation enhancement were found when cells themselves were injured. The results suggest that DNA lesions per se serve as a signal triggering the expression of enhanced viral mutagenesis. Because DNA of SV40 and calf thymus is unlikely to be replicated in the cells used, replication of damaged D N A might not be a prerequisite for the formation of the signal for enhanced mutagenesis. UV-damaged D N A present in a cell might be so processed that cellular factors which stimulate mutagenesis become available. 1 Cornelis, J.J., Z.Z. Su, D. Ward and J. Rommelaere, Proc. Natl. Acad. Sci. (U.S.A.), 78 (1981) 4480-4484.
7 M. Brugmans, H. Degreef I and H. van den Berghe, Division of Human Genetics, 1 Division of Dermatology, University of Leuven, Minderbroedersstraat 12, B-3000 Leuven
6 C. Dinsart, Z. Su, J. Cornelis and J. Rommelaere, Laboratoire de Biophysique et Radiobiologie, Universit~ Libre de Bruxelles, rue des Chevaux, 67, B-1640 RhodeSt-Gen~se
Extracellularly UV-damaged DNA induces mutations in intact parvovirus H-I infecting mammalian cells The frequency of mutants among the progeny of intact parvovirus H-1 is increased when cells are exposed to low doses of UV radiation or chemicals before virus infection. The same phenomenon is observed if cells are pretreated with UV-killed Simian virus 40 (SV40) or H-1 [1]. In a study on the nature of the signal that triggers the enhancement of viral mutagenesis, extracellularly UV-irradiated heterologous DNA from calf thymus or SV40 origin was introduced (by transfection) into undamaged human or rat cells before infection with a thermosensitive H-1 mutant. An enhanced number of wild-type virus revertants was produced in cells pretreated with UV-irradiated DNA as compared with controls infected with unirradiated DNA. About 2-fold increases in mutation frequency were observed; similar levels of mutation enhancement were found when cells themselves were injured. The results suggest that DNA lesions per se serve as a signal triggering the expression of enhanced viral mutagenesis. Because DNA of SV40 and calf thymus is unlikely to be replicated in the cells used, replication of damaged D N A might not be a prerequisite for the formation of the signal for enhanced mutagenesis. UV-damaged D N A present in a cell might be so processed that cellular factors which stimulate mutagenesis become available. 1 Cornelis, J.J., Z.Z. Su, D. Ward and J. Rommelaere, Proc. Natl. Acad. Sci. (U.S.A.), 78 (1981) 4480-4484.
7 M. Brugmans, H. Degreef I and H. van den Berghe, Division of Human Genetics, 1 Division of Dermatology, University of Leuven, Minderbroedersstraat 12, B-3000 Leuven