By D. Gale Johnson
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It is known that mutants of E. coli and B. sllbtilis exist in which increased susceptibility to irradiation and! or higher mutability is associated with deficiency in DNA polymerase or other key enzymes concerned with replication and repair of DNA. This, on the one hand, suggests that modification of such enzymes could be a means of controlling mutation rate and, on the other, that the evolution of these repair enzymes may have been necessary to counter the effect of radiation from the environment.
More than one weakness may playa part in the fatal outcome, but both old age and chronic tuberculosis are associated with depressed immune responses and it is simplest and probably correct to ascribe death to a failure of the immune reactions that were called for. 1 ' - - _ . 1 . - _ - ' - _ - ' - _ - - - ' - _ - - '_ _'---_'""'--_-'-o 10 2U 30 40 50 70 7S1 A~< (yn) Figure 8 The age-specific mortality in Victoria (Australia) for 1856-1858 and 1965-1967 to show the approximate straight line from 20--30 onwards when plotted in semi-logarithmic fashion.
The fidelity of DNA replication is vouched for in the control mutation rate in any quantitative experiment with extrinsic mutagens. Less than 100 per 108 duplications is a usual figure, and even with a potent mutagen like ultraviolet radiation the yield is rarely increased by more than two orders of magnitude. Another finding from bacterial genetics that is directly relevant to the broader theme is the regularity of the results when the error-proneness of the enzyme is increased, as in our instance where Zn is replaced with Mn.