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MINI-REVIEW

Rebuttal: Adaptive Mutation in Escherichia coli (Foster)

Microbiology Section, University of California, Davis, Davis, California 95616,¹ Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82 Solna,² Microbiology and Tumour Biology Center, Karolinska Institute, S-171 77, Solna Sweden³

If mutations arose in nongrowing cells, as proposed in Foster's paper (1), then stress-induced mutagenesis would seem inescapable. The plated population certainly grows very little. However, no evidence is provided that reversion occurs in this population and no effort is made to counter evidence to the contrary (see below)—that mutations actually arise in cells growing under selection within developing clones (rendering mutagenesis dispensable).

(i) Reversion requires that the lac allele be leaky and lactose be present in the selection medium, suggesting a growth requirement.

(ii) General mutagenesis is not induced by simple starvation (3) but is seen in the Cairns system when lactose is provided, suggesting dependence on growth.

(iii) Clonally related unstable and stable lac⁺ cells are found within all revertant colonies, consistent with both types arising sequentially within a growing colony.

(iv) Revertant number is strongly reduced if one inhibits growth of cells carrying a lac amplification.

(v) Revertant number increases if a lac duplication is provided in the parent cells.

(vi) Results of the respreading experiment are not inconsistent with reversion within growing clones because single duplication-bearing cells have a low (10^–4) probability of forming a visible revertant colony.

The genomic position of lac affects behavior of this system. Cited results suggest that general mutagenesis under selection is independent of lac position and therefore must reflect a genome-wide stress response. However, we have only seen general mutagenesis when the lac locus under selection is on the F'₁₂₈ plasmid located cis to dinB⁺ (allowing coamplification). It has also been argued that the lac reversion rate is 100-fold higher on F than in the chromosome, and the stress-induced increase is only apparent when applied to the higher basal lac rate on the plasmid (J. Cairns and P. L. Foster, Letter, Genetics 165:2317-2318, 2003). In contrast, we find the same lac reversion rate on F'₁₂₈ as at any of 30 chromosomal sites (J. R. Roth, E. Kofoid, F. P. Roth, O. G. Berg, J. Seger, and D. I. Andersson, Letter, Genetics 165:2319-2321, 2003). Both conflicts may reflect problems in the strain with a chromosomal lac allele (2, 5). The structure of F'₁₂₈ makes it unexpectedly difficult to move the triply marked lac allele from F'₁₂₈ to the chromosome.

The higher reversion rate of a tetA frameshift observed on F during selection may reflect coamplification of tetA with lac rather than mutation directed to F. Greater mutagenesis of F seems a minor point, since mutagenesis makes such a small contribution to reversion (see our rebuttal of Rosenberg and Hastings [6]).

Our experience with Salmonella suggests that the effect of an rpoS mutation on revertant number (seen in Escherichia coli) is likely to be indirect rather than an alteration of a programmed response to stress. It has previously been shown that this mutation reduces growth under selective conditions (4); alternatively, it could reduce the amplification rate, expression of the tra operon, or the extent of SOS induction.

	FOOTNOTES

 
* Corresponding author. Mailing address: University of California, Davis, Microbiology Section, One Shields Ave., Davis, CA 95616. Phone: (530) 752-6679. Fax: (530) 752-7663. E-mail: jrroth{at}ucdavis.edu.

REFERENCES

1. Foster, P. L. 2004. Adaptive mutation in Escherichia coli. J. Bacteriol. 186:4846-4852.[Free Full Text]
2. Foster, P. L., and J. M. Trimarchi. 1995. Adaptive reversion of an episomal frameshift mutation in Escherichia coli requires conjugal functions but not actual conjugation. Proc. Natl. Acad. Sci. USA 92:5487-5490.[Abstract/Free Full Text]
3. Hughes, D., and D. I. Andersson. 1997. Carbon starvation of Salmonella typhimurium does not cause a general increase of mutation rates. J. Bacteriol. 179:6688-6691.[Abstract/Free Full Text]
4. Lombardo, M.-J., I. Aponyi, and S. M. Rosenberg. 2004. General stress response regulator RpoS in adaptive mutation and amplification in Escherichia coli. Genetics 166:669-680.
5. Rosche, W. A., and P. L. Foster. 1999. The role of transient hypermutators in adaptive mutation in Escherichia coli. Proc. Natl. Acad. Sci. USA 96:6862-6867.[Abstract/Free Full Text]
6. Roth, J. R., and D. I. Andersson. 2004. Rebuttal: adaptive point mutation (Rosenberg and Hastings). J. Bacteriol. 186:4844.[Free Full Text]

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