Mammalian cells are able to repair damage to their DNA by a non-semiconservative mode of replication (repair replication, Rasmussen & Painter, 1964, 1966). Mengovirus and Newcastle disease virus are two cytocidal RNA viruses that inhibit semiconservative DNA replication soon after infection (Ensminger & Tamm, 1970a). Neither inhibits non-S phase or unscheduled DNA synthesis (Hand & Tamm, 1971), which probably represents a repair process (Painter & Cleaver, 1969). We have now examined repair replication in cells infected with mengovirus or Newcastle disease virus using more direct methods of measurement. If damaged DNA is labelled during repair with [3H]-bromodeoxyuridine (BrdUrd), the repaired regions are too short to produce a shift in density of the DNA and thus sediment as DNA of normal density when analysed by isopycnic sedimentation in caesium chloride (Pettijohn & Hanawalt, 1964; Cleaver, 1969b).
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