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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    32 DISCUSSION those conditions. She was in fact trying to interpret mutation frequency decline in terms of excision repair of the DNA, which I think is still the best working hypothesis. Auerbach: Why should it act specifically on suppressor mutations ? Bridges: Because when one takes tryptophan away the RC rei locus switches off transfer RNA and ribosomal RNA synthesis, but it doesn't cut off messenger RNA synthesis. One therefore wouldn't expect it to affect true mutations at loci where there is messenger synthesis. One would expect it to affect only suppressor mutations at loci where either transfer or ribosomal RNA is synthesized. S. Igali and I have been looking at this in a recently isolated relaxed mutant of WPa. When one removes trypto¬ phan, as one does in a mutation frequency decline experiment, RNA synthesis goes on at a much higher rate than in the normal (stringent) strain. Conversely, mutation frequency decline is slowed down in the relaxed strain to some extent. So there does seem to be an inverse con¬ nexion between the rate of transfer RNA and ribosomal RNA synthesis and the rate of mutation frequency decline, which would be consistent with Dr. Witkin's idea. MaaUe: You may be right, but when a relaxed strain has accumulated RNA of the stable kind, during starvation, then, for some time after the readdition of the amino acid both induction and derepression of enzyme synthesis are greatly inhibited. This has nothing to do with mutations; the inhibition phenomenon is transient, and it certainly has nothing to do with the need for making a new species of tRNA. This mysterious effect has been studied in detail by G. Turnock (unpubhshed). Bridges: It must presumably be something to do with the repressed state and what represses the transfer RNA locus. We don't know this of course. Clarke: Is the relaxed mutant in fact slower in MFD ? One would then suspect that an Mfd~ mutant might map in the RC locus. What I am really saying is that we should isolate Mfd mutants and map them. Bridges: Mapping doesn't necessarily tell you anything. Clarke: No, but if they all fall into the uvrA locus, that helps. Bridges: It is quite possible that Mfd~ mutants could be relaxed mutants although one we have recently examined was not. Witkin {Comments added in proof) : I do not agree with Dr. Clarke that the final nature of MFD is still vmclear. I think that the evidence over¬ whelmingly supports the interpretation that I offered several years ago: that MFD is a special case of excision repair, in which certain premutational u.V. photoproducts in suppressor genes (but not in most other genes) are excised only if protein synthesis is inhibited immediately after irradiation.