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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    DISCUSSION 15 infection by wild and c-type there was no indication that selection influenced the growth within the plaque. Loveless: If you give mixed infections of mutant and wild type do they emerge in the first burst in the same proportion as you have put them in ? If they don't, then your mixed infection experiments have no relevance. Kaplan: The proportion of wild to c-type in the mixed infection was 50:50, There was no marked difference in the plaques. Auerbach: Mosaics may be of two entirely different kinds. First, there may be a mutation in only one strand of DNA; this will usually lead to a large admixture of wild-type phage. Second, there are replicating in- stabihties ; these may give rise to clones with very few mutants. The issue becomes confused quantitatively if one pools the two types. Kaplan: This is an important point. There are two kinds of mixtures. In one an unstable allele may be produced which would mutate spon¬ taneously during the growth of the clone. In the other, stable types are produced which give a kind of segregation in the clone. Auerbach: In the organisms with which I am familiar the distinction is fairly easy. With phage one would have to see whether one and the same wild-type phage particle can give rise to several mutated ones, in which case it is an instability that can replicate as such. Kaplan: We made further post-cultures of the first progeny plates and noted whether plaques of wild type and of c-type were stable or not. We found only one case of instability in further post-cultures. All the cases shown in Table II (p. 9) are stable. We tested all types of clones. In the first series we only picked the c-plaques. But there was the mentioned deficit of clones with much wild type which was attributed to the fact that clones with an excess of wild type often look like wild-type plaques. Therefore a great number of wild-type plaques appearing after u.v. irradiation were picked. They contained in fact a few clones with a minority of mutants. We added these values to the distribution of the first series of pickings of c-plaques and got the distribution I showed in Fig. 3 (p. 11). Plaques with 40-50 per cent c-type look clearer than wild-type plaques. Evans: In Table II, Professor Kaplan, you showed that the percentage of mosaics decreased with increasing mutation frequency or increasing dose. This in fact agrees with one of the four hypotheses put forward to account for the origin of mosaics, as listed by Nasim and Auerbach (1967). Is the reverse of this result seen in Drosophila sperm in situations where there is no in-built replicating instabiUty, i.e. is there any evidence for an increasing percentage of mosaics with increasing dose ?