Abstract

Lesions that promote reversion from a temperature-sensitive to a wild-type phenotype were induced in temperature-sensitive late mutants of SV40 virus by UV irradiation. When cultures infected with UV-irradiated temperature-sensitive mutants were grown for various times at permissive temperature (32°C) and then at restrictive temperature (39°C), the reversion frequency declined just before the onset of semiconservative DNA synthesis when DNA synthesis began at 32°C. This decline can be explained by competition between reactions that lead to the onset of viral DNA synthesis and reactions that repair the lesions before the onset of viral DNA synthesis.

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