Mutation as cellular process : a Ciba Foundation symposium / edited by G.E.W. Wolstenholme and Maeve O'Connor.

  • Symposium on Mutation as Cellular Process (1969 : London, England)
Date:
1969
Catalogue details

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

Credit: Mutation as cellular process : a Ciba Foundation symposium / edited by G.E.W. Wolstenholme and Maeve O'Connor. Source: Wellcome Collection.

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    234 FINAL DISCUSSION Sobeh: Would you predict that the lethal hits have a higher dose expo¬ nent than the mutational damage? Auerbach: I think that dose-effect curves for mutations in cellular orga¬ nisms are composite curves, and that the dose exponents must be inter¬ preted with great caution. Sobels: In Drosophila one finds more completes at higher doses (Inagaki and Nakao, 1966). Auerbach: This may well be due to lethal hits, which certainly contribute to the completes. The only question is whether they can quantitatively account for them and for our data they can't. Apparently they can for Vielmetter's data. Sobels: What seems worth doing is to test whether a change occurs in the ratio of completes to mosaics in a system where straightforward repair can be measured. Auerbach: The trouble is that there are so many repair systems. Nasim tested two strains of Saccharomyces which are more u.v. sensitive than the wild type. They did produce more mosaics but the effect is not very striking. Sobels: How does the phenomenon of lethal sectoring which has been studied so extensively in yeast fit in with your ideas? Auerbach: That is the converse. A lethal sector is presumed to represent a lethal hit and therefore should lead to a complete mutation. Haefiier (1967) did a lot of this work, but we agreed that lethal sectors cannot explain all completes in fission yeast, although there is no doubt that they contri¬ bute to them. Dawson: In only two of the five systems of instability that we have looked at in Salmonella is there evidence which points in the direction of what we call controlling episomes. In the other three we have no evidence that the instability has a mechanism of that type. I am very conscious, in much of the discussion about replicating instabilities, of the inadequacy of the evidence for distinguishing between possible mechanisms. For example is it known, for the instabilities that are induced in Drosophila by chemical mutagens, whether the instability is even inherited at the gene whose instability you are scoring? May it not be, as in maize (McClintock, 1965) and delphinium (Dawson, 1964), that the instability is a two-element system and you have induced something at the regulator rather than at the gene whose phenotype you are scoring? Also one very seldom seems to know whether the instability is referrable to any particular site in the gene, or whether it is an instability over considerable regions of the genome. In much of the work that one hears discussed—mosaic colonies and so on—