Endurance of life : the implications of genetics for human life / Macfarlane Burnet.

  • Burnet, F. M. (Frank Macfarlane), Sir, 1899-1985.
Date:
1978
Catalogue details

Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Credit: Endurance of life : the implications of genetics for human life / Macfarlane Burnet. Source: Wellcome Collection.

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    3 A Persona! Approach 41 structure of E. coli. The scientific consensus was that biology is infinitely more complex than celestial dynamics and that the project was far too ambitious for this century. This however does not diminish the importance of testing genetic ideas on E. coli and one or two of the viruses than can live at its expense. Bacterial viruses are necessarily smaller and simpler in their genetic structure than bac¬ teria, and for some purposes they are even more suitable as a model on which to test genetic principles than £1 coli. It was with this model in fact that professional geneticists had already obtained the answer I was looking for, but in a quite different context from mammaUan ageing. It was found, in the course of an analysis of mutants, in the bacterial virus T4D. This is noplace for technical details of virus genetics. All that need be said is that it is possible to map, on the virus's circular double strands of DNA, the relative position of any gene identified by the occurrence of a mutation. Many of those genes, including No. 43, can be definitely identified as controlhng a particular enzyme. No. 43 con¬ trols a DNA polymerase, an enzyme, it will be remembered, whose function is to place the nucleotide units A, G, T, and С in the right places when a DNA strand is being duplicated or repaired. A large collection of mutants of the virus, all with the mutation proved to have involved gene 43, was accumulated and put through many tests. The only one that is relevant was to determine their mutability. Bacterial viruses are rather highly mutable objects and there are simple methods of determining the spontaneous rates at which several different types of mutants appear. If it is more relevant to the experiment, a mutagen like ultraviolet light can be used to increase the yield of mutants. With such tests it was found that there were several of these mutant strains that produced many more mutants than normal. A vital point was that the mutation rate was up, irrespective of what particular type of mutant was being looked for. These mutants were classed as mutator strains. Even more enlight¬ ening was the fact that two anti-mutator strains were found,^ which even under ultraviolet light exposure produced many less mutants than the normal virus. The only conclusion that could be drawn was that the normal strain- the wild type—has a DNA polymerase that, under control of its gene, makes a small proportion of genetic errors. If that gene is altered, the functional efficiency of the enzyme may be modified. For most mutants the alteration is as might be expected; if it has any effect on mutation rate at all it is towards inefficiency. More genetic errors occur and more mutants are isolated; the en¬ zyme has become more error-prone. But some rarer changes seem to make the enzyme less error-prone. Taken at face value, these ex-