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Author: coolerthanranch Add to my Favorite Fools Ignore this person (you won't see their posts anymore) Number: of 25060  
Subject: Re: Non-random mutation? Date: 10/22/2001 2:27 PM
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Recommendations: 2
Cairns himself disavowed his original 'conclusions' - amazingly, after more research had been done. More up to date research indicates that the phenomenon is, in fact, genome wide mutation as a result of oxidative stress.

Mutat Res 1999 Jul;437(1):51-60
Mismatch repair is diminished during stationary-phase mutation.

Harris RS, Feng G, Ross KJ, Sidhu R, Thulin C, Longerich S, Szigety SK, Hastings PJ, Winkler ME,Rosenberg SM.

Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA.

This paper is an invited Response to a recent Commentary [P.L. Foster, Rev. Mut. Res. 436 (1999) 179-184] entitled "Are adaptive mutations due to a decline in mismatch repair? The evidence is lacking". The Commentary argues that no evidence exists supporting the idea that mismatch repair is limiting specifically during stationary-phase mutation. A primary concern of the author is to question the method that we used previously to measure growth-dependent mutation. In this method, mutation rates are calculated using counts of mutant colonies taken at times when those colonies arise, rather than at a predetermined, fixed time. Here we show further data that illustrate why this must be done to ensure accurate mutation measurements. Such accuracy was necessary for our published determination that mismatch repair proteins are not limiting during growth-dependent mutation, but become so during stationary-phase mutation. We review the evidence supporting the idea that stationary-phase reversion of a lac frameshift mutation occurs in an environment of decreased mismatch repair capacity. Those data are substantial. The data presented in the Commentary, in apparent contradiction to this idea, do not justify the conclusion presented there. Copyright 1999 Elsevier Science B.V.

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Ann N Y Acad Sci 1999 May 18;870:275-89
Mechanisms of genome-wide hypermutation in stationary phase.

Lombardo MJ, Torkelson J, Bull HJ, McKenzie GJ, Rosenberg SM.

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030-3498, USA.

Stationary-phase mutation (a subset of which was previously called adaptive mutation) occurs in apparently nondividing, stationary-phase cells exposed to a nonlethal genetic selection. In one experimental system, stationary-phase reversion of an Escherichia coli F'-borne lac frameshift mutation occurs by a novel molecular mechanism that requires homologous recombination functions of the RecBCD system. Chromosomal mutations at multiple loci are detected more frequently in Lac+ stationary-phase revertants than in cells that were also exposed to selection but did not become Lac+. Thus, mutating cells represent a subpopulation that experiences hypermutation throughout the genome. This paper summarizes current knowledge regarding stationary-phase mutation in the lac system. Hypotheses for the mechanism of chromosomal hypermutation are discussed, and data are presented that exclude one hypothetical mechanism in which chromosomal mutations result from Hfr formation.

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Science 1998 Nov 6;282(5391):1133-5
Evidence that gene amplification underlies adaptive mutability of the bacterial lac operon.

Andersson DI, Slechta ES, Roth JR.

Department of Biology, University of Utah, Salt Lake City, UT 84112, USA.

Adaptive mutability is the apparent alteration in specificity or rate of mutability seen in bacteria during stress. A model is proposed by which gene amplification during selective growth can give the appearance of adaptive mutability without requiring any change in mutability. The model is based on two assumptions, that a mutant lac locus with residual function allows growth if its copy number is increased, and that true reversion events are made more likely by replication of chromosomes with many copies of the locus. Apparent directed mutability, its recombination requirement, and its apparent independence of cell growth are all accounted for by the model. Evidence is provided for the required residual function and gene amplification.

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Mutat Res 1997 Apr 14;375(1):19-24
A direct role for DNA polymerase III in adaptive reversion of a frameshift mutation in Escherichia coli.

Harris RS, Bull HJ, Rosenberg SM.

Department of Biochemistry, University of Alberta Faculty of Medicine, Edmonton, Canada.

The sequences of adaptive reversions of a lac frameshift mutation in Escherichia coli resemble DNA polymerase errors, and the adaptive reversions decrease in strains with an antimutator DNA polymerase III(PolIII) allele. The latter finding could imply that DNA PolIII itself makes adaptive mutations. Alternatively,normal DNA PolIII errors could saturate post-synthesis mismatch repair during adaptive mutation. If so, the antimutator strain would produce fewer adaptive mutations because it possesses greater capacity for mismatch repair which could correct errors made by a polymerase other than DNA PolIII. Mismatch repair capacity is limited specifically during adaptive mutation, necessitating a test of this indirect model. This indirect model is ruled out here by the observation that the antimutator PolIII allele decreases adaptive mutation even in mismatch repair-defective cells. This supports a direct role for DNA PolIII in recombination-dependent adaptive mutation.

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Annu Rev Genet 1999;33:57-88
Mechanisms of stationary phase mutation: a decade of adaptive mutation.

Foster PL.

Department of Biology, Indiana University, Bloomington 47405, USA. pfoster@bio.indiana.edu

A decade of research on adaptive mutation has revealed a plethora of mutagenic mechanisms that may be important in evolution. The DNA synthesis associated with recombination could be an important source of spontaneous mutation in cells that are not proliferating. The movement of insertion elements can be responsive to environmental conditions. Insertion elements not only activate and inactivate genes, they also provide sequence homology that allows large-scale genomic rearrangements. Some conjugative plasmids can recombine with their host's chromosome, and may acquire chromosomal genes that could then spread through the population and even to other species. Finally, a subpopulation of transient hypermutators could be a source of multiple variant alleles, providing a mechanism for rapid evolution under adverse conditions.

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And since you think Foster has something important to say:

Mutat Res 2001 Jan 25;473(1):109-19
Effect of endogenous carotenoids on "adaptive" mutation in Escherichia coli FC40.

Bridges BA, Foster PL, Timms AR.

MRC Cell Mutation Unit, University of Sussex, Falmer, BN1 9RR, Brighton, UK. b.a.bridges@sussex.ac.uk

The appearance over many days of Lac(+) frameshift mutations in Escherichia coli strain FC40 incubated on lactose selection plates is a classic example of apparent "adaptive" mutation in an episomal gene. We show that endogenously overproduced carotenoids reduce adaptive mutation under selective conditions by a factor of around two. Carotenoids are known to scavenge singlet oxygen suggesting that the accumulation of oxidative base damage may be an integral part of the adaptive mutation phenomenon. If so, the lesion cannot be 7,8-dihydro-8-oxoguanine since adaptive mutation in FC40 is unaffected by mutM and mutY mutations. If active oxygen species such as singlet oxygen are involved in adaptive mutation then they should also induce frameshift mutations in FC40 under non-selective conditions. We show that such mutations can be induced under non-selective conditions by protoporphyrin photosensitisation and that this photodynamic induction is reduced by a factor of just over two when endogenous carotenoids are present. We argue that the involvement of oxidative damage would in no way be inconsistent with current understanding of the mechanism of adaptive mutation and the role of DNA polymerases.

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There are more, of course, and all after Cairns' original paper.

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