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Cell division and DNA synthesis were studied during axenic growth following 254 nm ultraviolet light (UV) irradiation of a repair‐proficient parental strain (rad+, D10 colony formation = 195 J/m2) and two repair mutants (radC. D10= 50 J/m2; radB. D10= 5 J/m2) of Dictyostelium discoideum. Isopycnic CsCI gradients were used to distinguish uptake of labeled precursors into nuclear (n) and mitochondrial (m) DNA, using Netropsin to enhance the density resolution. In all strains, m‐DNA synthesis was inhibited to a lesser extent than was n‐DNA synthesis. For radC, which has been shown in other experiments to be slow in incision and dimer removal, the UV‐induced lags in division and n‐DNA synthesis were longer than for rad+. However, radB showed a more complex response. Although brief division lags were observed for < 10 J/m2, little immediate division lag was detected at greater fluences. Instead, a brief period of cell multiplication of up to but not exceeding two‐fold occurred, followed by a cessation of division, and then by lysis. Fluences that yielded extensive lags in n‐DNA synthesis in rad‐ and radC resulted in little detectable immediate postirradiation lag in n‐DNA synthesis in radB. However, later in the postirradiation period, when DNA synthesis had resumed in rad+ and radC. it gradually declined to near zero in radB. We conclude: (1) that the more extended lag in division and n‐DNA synthesis in radC is consistent with its slower rate of excision repair, and (2) that radB contains a defect resulting in less initial blockage of DNA replication by UV lesions.
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Kielman et al. (1980) studied this question.
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