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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    FINAL DISCUSSION 233 Kimball: There is trouble with the repair hypothesis. It necessitates that the mutation be fixed at the time of repair, in some sense, because the whole hypothesis depends on putting in the wrong bases at the time of repair. It seems to me there is fairly good evidence firom Witkin's work (1967) on the Rec~ mutations, with and without excision repair operating, that con¬ siderable amounts of repair can go on with no mutation production what¬ soever. Also some of our data with Paramecium (Kimball, 1966) suggest rather strongly that the major source of mutation is not fixation at the time of repair but fixation at or near the time of replication. Yet mutations in this organism are primarily complete and not partial. Auerbach: We don't know whether dark repair occurs in Schizo- saccharomyces. Clarke: We do know that dark repair occurs in Schizosaccharomyces pombe u.V. mutants. Kimball: I think we have to accept in any repair hypothesis that mutation is fixed at the time of repair. It seems to me that this is essential to the whole thing. If there is little or no fixation of mutation at the time of repair then I have great problems with the hypothesis. Auerbach: What do you mean by fixation? Do you mean insertion of a mutated base? Kimball: In the repair hypothesis one puts in the wrong base. Once you have got that far the mutation is there in the replicating form. MaaUe: In later studies Vielmetter, Messer and Schütte (1968) observed systematic changes in the ratio of solid versus solid+sectored colonies as a function of the map position of the character they looked at. This does not fit the lethal-hit notion, in the sense that if one considers a locus close to the origin of replication most of the cells in the population will carry two copies of this locus and vice versa for positions close to the end of the replicating unit. From this one can work out an expectancy for sectored colonies among all colonies at any time subsequent to the mutagenic event. Kubitschek: It seems to me that one can explain mosaicism on a master strand model by assuming that repair occurs in some subsequent generation. We know that repair can occur after the first division from the work of Bridges and Munson (1968) and from Sauerbier's work (Sauerbier and Hirsch-Kauffmann, 1968) with phage, for example, where thymine dimers are carried through to the progeny. Auerbach: If I have to make assumptions I prefer to make one rather than two. I have only to assume repair and you have to assume both master strand and repair.