DNA-repair mechanisms : symposium, Schloss Reinhartshausen/Rhein, Oct. 4th/5th, 1971 / chairman H. Altmann.

Date:
[1972]
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Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: DNA-repair mechanisms : symposium, Schloss Reinhartshausen/Rhein, Oct. 4th/5th, 1971 / chairman H. Altmann. Source: Wellcome Collection.

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    Fig. 4. Typical survival curves of the haploid spore clone 289-4c carrying the r®-gene after X irradiation in oxygenated (points) and hypoxic conditions (triangles) after im mediate plating (full lines) and 48 hours agar-holding (AHR, dotted lines). Percentage of budding cells in the irradiated sample 6.8%. Lindahl : DNA-repair mechanisms have presumably evolved in response to the most common types of damage to intracellular DNA. One such form of damage is probably that due to heat. On heating DNA in solution at a temperature below the T m , a slow degradation of the primary structure takes place, mainly due to depurination [Greer, S. and S. Zamenhof: J. molec. Biol. 4: 123 (1962)]. The temperature dependence of this inactivation of double-stranded DNA has been determined by following the rate of loss of transforming activity at different temperatures, and by direct measurements of the rate of release of purine bases from DNA radioactively labelled in these residues [Lindahl, T. and B. Nyberg: Biochemistry, in press (1972)]. For the latter type of experiments, DNA was isolated from a purine-dependent mutant strain of B. subtilis grown in the presence of 14 C-adenine. The data available so far indicate that at neutral pH and ionic strength 0.15, 1 purine base is released per 10 6 -10 7 base pairs per hour at 37°C. It seems