Rebuttal: adaptive point mutation (Rosenberg and Hastings).
Rebuttal: adaptive point mutation (Rosenberg and Hastings).
复制标题
反驳:适应性点突变(Rosenberg 和 Hastings)。
DOI:
10.1128/jb.186.15.4845.2004
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发表时间:
2004
影响因子:
3.2
通讯作者:
Foster,PatriciaL
中科院分区:
文献类型:
--
作者:
Foster,PatriciaL
Rosenberg and Hastings (4) commit the same logical fallacy as do Roth and Andersson (5). They first state that there are three models to explain adaptive mutation: directed mutation, hypermutation, and cryptic growth. Then they argue against directed mutation and cryptic growth, leaving hypermutation as the only alternative. But, they ignore the alternative model that I presented in my review (2), which involves neither directed mutation nor cryptic growth. My model postulates one underlying mutational mechanism in which all cells can engage; but, in a few cells (the hypermutators) the process is more mutagenic than in the majority because Pol IV is highly expressed and mismatch repair is deficient. The majority produces 90% and the hypermutators produce 10% of the Lac mutations, but hypermutators produce all of the multiple mutations.The conclusion that only a few Lac mutations arise in hypermutators is based, in part, on the higher than expected frequency of Lac cells with two other mutations. Rosenberg and Hastings argue that this is because some cells spend more time in the hypermutable state and thus have more mutations. It is true that the proportion of cells with multiple mutations increases with time during lactose selection (3). But this effect is not large enough to account for the frequency of triple mutants. The argument is as follows (J. Cairns, personal communication).