1887
No metrics data to plot.
The attempt to load metrics for this article has failed.
The attempt to plot a graph for these metrics has failed.

EcoSal Plus

Domain 6:

Evolution and Genomics

The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection

MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.
Buy article
Choose downloadable ePub or PDF files.
Buy this Chapter
Digital (?) $30.00
  • Authors: Dan I. Andersson1, Diarmaid Hughes2, and John R. Roth3
  • Editor: James M. Slauch4
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Department of Medical Biochemistry and Microbiology, Uppsala University, S-75123 Uppsala, and Department of Cell and Molecular Biology, Uppsala University, S-75124 Uppsala, Sweden, and Department of Microbiology, CBS, University of California—Davis, Davis, CA 95616; 2: Department of Medical Biochemistry and Microbiology, Uppsala University, S-75123 Uppsala, and Department of Cell and Molecular Biology, Uppsala University, S-75124 Uppsala, Sweden, and Department of Microbiology, CBS, University of California—Davis, Davis, CA 95616; 3: Department of Medical Biochemistry and Microbiology, Uppsala University, S-75123 Uppsala, and Department of Cell and Molecular Biology, Uppsala University, S-75124 Uppsala, Sweden, and Department of Microbiology, CBS, University of California—Davis, Davis, CA 95616; 4: The Schoold of Molecular and Cellular Biology, University of Illinois at Urbana-Champaign, Urbana, IL
  • Received 12 January 2010 Accepted 16 March 2010 Published 17 March 2011
  • Address correspondence to Dan I. Andersson Dan.Andersson@imbim.uu.se
image of The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection
    Preview this reference work article:
    Zoom in
    Zoomout

    The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, Page 1 of 2

    | /docserver/preview/fulltext/ecosalplus/4/2/5_6_6_module-1.gif /docserver/preview/fulltext/ecosalplus/4/2/5_6_6_module-2.gif
  • Abstract:

    The classical experiments of Luria and Delbrück showed convincingly that mutations exist before selection and do not contribute to the creation of mutations when selection is lethal. In contrast, when nonlethal selections are used,measuring mutation rates and separating the effects of mutation and selection are difficult and require methods to fully exclude growth after selection has been applied. Although many claims of stress-induced mutagenesis have been made, it is difficult to exclude the influence of growth under nonlethal selection conditions in accounting for the observed increases in mutant frequency. Instead, for many of the studied experimental systems the increase in mutant frequency can be explainedbetter by the ability of selection to detect small differences in growth rate caused by common small effect mutations. A verycommon mutant class,found in response to many different types of selective regimensin which increased gene dosage can resolve the problem, is gene amplification. In the well-studied system of Cairns and Foster, the apparent increase in Lac+revertants can be explained by high-level amplification of the operon and the increased probability for a reversion mutation to occur in any one of the amplified copies. The associated increase in general mutation rate observed in revertant cells in that system is an artifact caused by the coincidental co-amplification of the nearby gene (encoding the error-prone DNA polymerase IV) on the particular plasmid used for these experiments. Apart from the system, similar gene amplification processes have been described for adaptation to toxic drugs, growth in host cells, and various nutrient limitations.

  • Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6

Key Concept Ranking

DNA Polymerase IV
0.42957708
Frameshift Mutation
0.4137164
Gene Duplication
0.41012615
Nucleotide Excision Repair
0.4089339
Deletion Mutation
0.4052137
0.42957708

References

1. Lederberg J, Lederberg EM. 1952. Replica plating and indirect selection of bacterial mutants. J Bacteriol 63:399–406.[PubMed]
2. Luria SE, Delbrück M. 1943. Mutations of bacteria from virus sensitivity to virus resistance. Genetics 28:491–511.[PubMed]
3. Feng G, Tsui HC, Winkler ME. 1996. Depletion of the cellular amounts of the MutS and MutH methyl-directed mismatch repair proteins in stationary-phase Escherichia coli K-12 cells. J Bacteriol 178:2388–2396.[PubMed]
4. Harris RS, Feng G, Ross KJ, Sidhu R, Thulin C, Longerich S, Szigety SK, Winkler ME, Rosenberg SM. 1997. Mismatch repair protein MutL becomes limiting during stationary-phase mutation. Genes Dev 11:2426–2437.[PubMed][CrossRef]
5. Bhagwat AS, Lieb M. 2002. Cooperation and competition in mismatch repair: very short-patch repair and methyl-directed mismatch repair in Escherichia coli. Mol Microbiol 44:1421–1428.[PubMed][CrossRef]
6. Drotschmann K, Aronshtam A, Fritz HJ, Marinus MG. 1998. The Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA. Nucleic Acids Res 26:948–953.[PubMed][CrossRef]
7. Mayr E. 1982. The Growth of Biological Thought: Diversity, Evolution, and Inheritance, p 738–744. Harvard University Press, Cambridge, MA.
8. Cairns J, Overbaugh J, Miller S. 1988. The origin of mutants. Nature 335:142–145.[PubMed][CrossRef]
9. Hall BG. 1988. Adaptive evolution that requires multiple spontaneous mutations. I. Mutations involving an insertion sequence. Genetics 120:887–897.[PubMed]
10. Shapiro JA. 1984. Observations on the formation of clones containing araB-lacZ cistron fusions. Mol Gen Genet 194:79–90.[PubMed][CrossRef]
11. Foster PL. 2007. Stress-induced mutagenesis in bacteria. Crit Rev Biochem Mol Biol 42:373–397.[PubMed][CrossRef]
12. Galhardo RS, Hastings PJ, Rosenberg SM. 2007. Mutation as a stress response and the regulation of evolvability. Crit Rev Biochem Mol Biol 42:399–435.[PubMed][CrossRef]
13. Freeland SJ, Hurst LD. 1998. The genetic code is one in a million. J Mol Evol 47:238–248.[PubMed][CrossRef]
14. Freeland SJ, Hurst LD. 2004. Evolution encoded. Sci Am 290:84–91.[PubMed][CrossRef]
15. Leong PM, Hsia HC, Miller JH. 1986. Analysis of spontaneous base substitutions generated in mismatch-repair-deficient strains of Escherichia coli. J Bacteriol 168:412–416.[PubMed]
16. Li W-H, Graur D. 2000. Fundamentals of Molecular Evolution, 2nd ed. Sinauer Associates, Sunderland, MA.
17. Markiewicz P, Kleina LG, Cruz C, Ehret S, Miller JH. 1994. Genetic studies of the lac repressor. XIV Analysis of 4000 altered Escherichia coli lac repressors reveals essential and non-essential residues, as well as “spacers” which do not require a specific sequence. J Mol Biol 240:421–433.[PubMed][CrossRef]
18. Miller JH. 1980. Genetic analysis of the lac repressor. Curr Top Microbiol Immunol 90:1–18.[PubMed]
19. Miller JH. 1983. Mutational specificity in bacteria. Annu Rev Genet 17:215–238.[PubMed][CrossRef]
20. Reams AB, Kofoid E, Savageau M, Roth JR. 2010. Duplication frequency in a population of Salmonella enterica rapidly approaches steady state with or without recombination. Genetics 184:1077–1094.
21. Rosche WA, Foster PL. 2000. Determining mutation rates in bacterial populations. Methods20:4–17.[PubMed][CrossRef]
22. Akerlund T, Nordstrom K, Bernander R. 1995. Analysis of cell size and DNA content in exponentially growing and stationary-phase batch cultures of Escherichia coli. J Bacteriol 177:6791–6797.[PubMed]
23. Hall BG. 1990. Spontaneous point mutations that occur more often when advantageous than when neutral. Genetics 126:5–16.[PubMed]
24. Hughes D, Andersson DI. 1997. Carbon starvation of Salmonella typhimurium does not cause a general increase of mutation rates. J Bacteriol 179:6688–6691.[PubMed]
25. Cairns J, Foster PL. 1991. Adaptive reversion of a frameshift mutation in Escherichia coli. Genetics 128:695–701.[PubMed]
26. Anderson P, Roth J. 1981. Spontaneous tandem genetic duplications in Salmonella typhimurium arise by unequal recombination between rRNA (rrn) cistrons. Proc Natl Acad Sci USA 78:3113–3117.[PubMed][CrossRef]
27. Kugelberg E, Kofoid E, Andersson DI, Lu Y, Mellor J, Roth FP, Roth JR. 2010. The tandem inversion duplication in Salmonella enterica: selection drives unstable precursors to final mutation types. Genetics 185:65–85.
28. Kugelberg E, Kofoid E, Reams AB, Andersson DI, Roth JR. 2006. Multiple pathways of selected gene amplification during adaptive mutation. Proc Natl Acad Sci USA 103:17319–17324.[PubMed][CrossRef]
29. Andersson DI, Slechta ES, Roth JR. 1998. Evidence that gene amplification underlies adaptive mutability of the bacterial lac operon. Science 282:1133–1135.[PubMed][CrossRef]
30. Hastings PJ. 2007. Adaptive amplification. Crit Rev Biochem Mol Biol 42:271–283.[PubMed][CrossRef]
31. Kim SR, Matsui K, Yamada M, Gruz P, Nohmi T. 2001. Roles of chromosomal and episomal dinB genes encoding DNA pol IV in targeted and untargeted mutagenesis in Escherichia coli. Mol Genet Genom 266:207–215.[PubMed][CrossRef]
32. Shapiro JA, Brinkley PM. 1984. Programming of DNA rearrangements involving Mu prophages. Cold Spring Harbor Symp Quant Biol 49:313–320.
33. Foster PL, Cairns J. 1994. The occurrence of heritable Mu excisions in starving cells of Escherichia coli. EMBO J 13:5240–5244.
34. Maenhaut-Michel G, Blake CE, Leach DR, Shapiro JA. 1997. Different structures of selected and unselected araB-lacZ fusions. Mol Microbiol 23:1133–1145.
35. Maenhaut-Michel G, Shapiro JA. 1994. The roles of starvation and selective substrates in emergence of araB-lacZ fusion clones. EMBO J 13:5229–5239.
36. Garibyan L, Huang T, Kim M, Wolff E, Nguyen A, Nguyen T, Diep A, Hu K, Iverson A, Yang H, Miller JH. 2003. Use of the rpoB gene to determine the specificity of base substitution mutations on the Escherichia coli chromosome. DNA Repair (Amst.) 2:593–608.[PubMed][CrossRef]
37. Taddei F, Matic I, Radman M. 1995. cAMP-dependent SOS induction and mutagenesis in resting bacterial populations. Proc Natl Acad Sci USA 92:11736–11740.[PubMed][CrossRef]
38. Taddei F, Halliday JA, Matic I, Radman M. 1997. Genetic analysis of mutagenesis in aging Escherichia coli colonies. Mol Gen Genet 256:277–281.[PubMed][CrossRef]
39. Bjedov I, Tenaillon O, Gerard B, Souza V, Denamur E, Radman M, Taddei F, Matic I. 2003. Stress-induced mutagenesis in bacteria. Science 300:1404–1409.[PubMed][CrossRef]
40. Wrande M, Roth JR, Hughes D. 2008. Accumulation of mutants in “aging” bacterial colonies is due to growth under selection, not stress-induced mutagenesis. Proc Natl Acad Sci USA 105:11863–11868.[PubMed][CrossRef]
41. Sun S, Berg OG, Roth JR, Andersson DI. 2009. Contribution of gene amplification to evolution of increased antibiotic resistance in Salmonella typhimurium. Genetics182:1183–1195.
42. Fisher RF, Yanofsky C. 1983. Mutations of the beta subunit of RNA polymerase alter both transcription pausing and transcription termination in the trp operon leader region in vitro. J Biol Chem 258:8146–8150.[PubMed]
43. Jin DJ, Gross CA. 1988. Mapping and sequencing of mutations in the Escherichia coli rpoB gene that lead to rifampicin resistance. J Mol Biol 202:45–58.[PubMed][CrossRef]
44. Jin DJ, Gross CA. 1991. RpoB8, a rifampicin-resistant termination-proficient RNA polymerase, has an increased Km for purine nucleotides during transcription elongation. J Biol Chem 266:14478–14485.[PubMed]
45. Landick R, Stewart J, Lee DN. 1990. Amino acid changes in conserved regions of the beta-subunit of Escherichia coli RNA polymerase alter transcription pausing and termination. Genes Dev 4:1623–1636.[PubMed][CrossRef]
46. Sagitov V, Nikiforov V, Goldfarb A. 1993. Dominant lethal mutations near the 5′ substrate binding site affect RNA polymerase propagation. J Biol Chem 268:2195–2202.[PubMed]
47. Singer M, Jin DJ, Walter WA, Gross CA. 1993. Genetic evidence for the interaction between cluster I and cluster III rifampicin resistant mutations. J Mol Biol 231:1–5.[PubMed][CrossRef]
48. Yanofsky C, Horn V. 1981. Rifampin resistance mutations that alter the efficiency of transcription termination at the tryptophan operon attenuator. J Bacteriol 145:1334–1341.[PubMed]
49. Hall BG. 1993. The role of single-mutant intermediates in the generation of trpAB double revertants during prolonged selection. J Bacteriol 175:6411–6414.[PubMed]
50. Hall BG. 1995. Adaptive mutations in Escherichia coli as a model for the multiple mutational origins of tumors. Proc Natl Acad Sci USA 92:5669–5673.[PubMed][CrossRef]
51. Hall BG. 1997. On the specificity of adaptive mutations. Genetics 145:39–44.[PubMed]
52. Hall BG. 1998. Adaptive mutagenesis at ebgR is regulated by PhoPQ. J Bacteriol 180:2862–2865.[PubMed]
53. Hall BG. 1991. Adaptive evolution that requires multiple spontaneous mutations: mutations involving base substitutions. Proc Natl Acad Sci USA 88:5882–5886.[PubMed][CrossRef]
54. Hall BG. 1999. Spectra of spontaneous growth-dependent and adaptive mutations at ebgR. J Bacteriol 181:1149–1155.[PubMed]
55. Hall BG. 1998. Activation of the bgl operon by adaptive mutation. Mol Biol Evol 15:1–5.[PubMed]
56. Loewe L, Textor V, Scherer S. 2003. High deleterious genomic mutation rate in stationary phase of Escherichia coli. Science 302:1558–1560.[PubMed][CrossRef]
57. de Visser JA, Rozen DE. 2004. Comment on “High deleterious genomic mutation rate in stationary phase of Escherichia coli.” Science 304:518; author reply 518.[PubMed][CrossRef]
58. Finkel SE, Kolter R. 1999. Evolution of microbial diversity during prolonged starvation. Proc Natl Acad Sci USA 96:4023–4027.[PubMed][CrossRef]
59. Zambrano MM, Kolter R. 1996. GASPing for life in stationary phase. Cell 86:181–184.[PubMed][CrossRef]
60. Pedraza-Reyes M, Yasbin RE. 2004. Contribution of the mismatch DNA repair system to the generation of stationary-phase-induced mutants of Bacillus subtilis. J Bacteriol 186:6485–6491.[PubMed][CrossRef]
61. Sung HM, Yasbin RE. 2002. Adaptive, or stationary-phase, mutagenesis, a component of bacterial differentiation in Bacillus subtilis. J Bacteriol 184:5641–5653.[PubMed][CrossRef]
62. Sung HM, Yeamans G, Ross CA, Yasbin RE. 2003. Roles of YqjH and YqjW, homologs of the Escherichia coli UmuC/DinB or Y superfamily of DNA polymerases, in stationary-phase mutagenesis and UV-induced mutagenesis of Bacillus subtilis. J Bacteriol 185:2153–2160.[PubMed][CrossRef]
63. Ross C, Pybus C, Pedraza-Reyes M, Sung HM, Yasbin RE, Robleto E. 2006. Novel role of mfd: effects on stationary-phase mutagenesis in Bacillus subtilis. J Bacteriol 188:7512–7520.[PubMed][CrossRef]
64. Davis BD. 1989. Transcriptional bias: a non-Lamarckian mechanism for substrate-induced mutations. Proc Natl Acad Sci USA 86:5005–5009.[PubMed][CrossRef]
65. Selby CP, Sancar A. 1993. Molecular mechanism of transcription-repair coupling. Science 260:53–58.[PubMed][CrossRef]
66. Steele DF, Jinks-Robertson S. 1992. An examination of adaptive reversion in Saccharomyces cerevisiae. Genetics 132:9–21.[PubMed]
67. Lea DE, Coulson CA. 1949. The distribution of numbers of mutants in bacterial populations. J Genet 49:264–285. [CrossRef]
68. Heidenreich E, Wintersberger U. 2001. Adaptive reversions of a frameshift mutation in arrested Saccharomyces cerevisiae cells by simple deletions in mononucleotide repeats. Mutat Res 473:101–107.[PubMed]
69. Yang Z, Lu Z, Wang A. 2001. Study of adaptive mutations in Salmonella typhimurium by using a super-repressing mutant of a trans regulatory gene purR. Mutat Res 484:95–102.[PubMed]
70. Yang Z, Lu Z, Wang A. 2006. Adaptive mutations in Salmonella typhimurium phenotypic of purR super-repression. Mutat Res 595:107–116.[PubMed]
71. Paulander W, Maisnier-Patin S, Andersson DI. 2007. Multiple mechanisms to ameliorate the fitness burden of mupirocin resistance in Salmonella typhimurium. Mol Microbiol 64:1038–1048.[PubMed][CrossRef]
72. Fojo T. 2007. Multiple paths to a drug resistance phenotype: mutations, translocations, deletions and amplification of coding genes or promoter regions, epigenetic changes and microRNAs. Drug Resist Updat 10:59–67.[PubMed][CrossRef]
73. Albertson DG. 2006. Gene amplification in cancer. Trends Genet 22:447–455.[PubMed][CrossRef]
ecosalplus.5.6.6.citations
ecosalplus/4/2
content/journal/ecosalplus/10.1128/ecosalplus.5.6.6
Loading

Citations loading...

Loading

Article metrics loading...

/content/journal/ecosalplus/10.1128/ecosalplus.5.6.6
2011-03-17
2017-07-20

Abstract:

The classical experiments of Luria and Delbrück showed convincingly that mutations exist before selection and do not contribute to the creation of mutations when selection is lethal. In contrast, when nonlethal selections are used,measuring mutation rates and separating the effects of mutation and selection are difficult and require methods to fully exclude growth after selection has been applied. Although many claims of stress-induced mutagenesis have been made, it is difficult to exclude the influence of growth under nonlethal selection conditions in accounting for the observed increases in mutant frequency. Instead, for many of the studied experimental systems the increase in mutant frequency can be explainedbetter by the ability of selection to detect small differences in growth rate caused by common small effect mutations. A verycommon mutant class,found in response to many different types of selective regimensin which increased gene dosage can resolve the problem, is gene amplification. In the well-studied system of Cairns and Foster, the apparent increase in Lac+revertants can be explained by high-level amplification of the operon and the increased probability for a reversion mutation to occur in any one of the amplified copies. The associated increase in general mutation rate observed in revertant cells in that system is an artifact caused by the coincidental co-amplification of the nearby gene (encoding the error-prone DNA polymerase IV) on the particular plasmid used for these experiments. Apart from the system, similar gene amplification processes have been described for adaptation to toxic drugs, growth in host cells, and various nutrient limitations.

Highlighted Text: Show | Hide
Loading full text...

Full text loading...

Comment has been disabled for this content
Submit comment
Close
Comment moderation successfully completed

Figures

Image of Figure 1
Figure 1

In the absence of selection, new mutants accumulate linearly with time. When selection acts, it causes an exponential increase in the frequency of a beneficial mutation. Thus, in a natural population, where both selection and mutation occur together, the frequency of a favorable mutant is more heavily impacted by selection than by recurring mutational events. It is often difficult to appreciate how powerful exponential increases can be.

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 2
Figure 2

The vertical axis is a list of all the genotypes present when a population is initiated. Mutation may change the nature of a particular lineage and the relative size of each lineage may change because of differences in their relative growth rate. Lineage size (log cell number) is depicted by the thickness of horizontal lines—some dwindle and some increase exponentially. Dashed lines indicate lineages altered by mutation but unaffected in growth rate.

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 3
Figure 3

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 4
Figure 4

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 5
Figure 5

During growth under selection, common small-effect mutations increase in frequency exponentially and expand clones large enough to allow secondary improvements to occur.

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 6
Figure 6

Selection is cleanly and completely separated from growth and mutation. Mutations are allowed to accumulate (linearly) during the initial nonselective pregrowth period. Precautions eliminate the effect of fluctuation or stochastic distribution of times at which mutations arise. Samples of nonselective growth culture are plated under strong selective conditions that block all growth of the parent type and all of the common small-effect mutations. Only rare large-effect mutations are allowed to grow under selection. These mutations are assumed to be fully fit and require no adaptive change to be detected on the selection plate.

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 7
Figure 7

The population diagrammed here reaches a plateau (10/ml) when some resource is exhausted. A mutant formed during the prior growth continues to divide (in this example for an additional 27 generations, resulting in a doubling of the total population).

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 8
Figure 8

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 9
Figure 9

As in the Luria-Delbrück experiment, parent cells are plated on selective medium mutant (revertant) colonies appear with time. These colonies have been attributed to mutations induced by stress in the nongrowing parent population. The main features of the Cairns-Foster experiment are described in the text and then discussed in terms of models offered to explain them.

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 10
Figure 10

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 11
Figure 11

Most Rif mutants are found to be localized as jackpots in one or a few sectors of the colony, and within each of these jackpots the mutants carry the same sequence alteration, consistent with selective growth of a Rif mutant during the period of “aging.” Adapted from reference 41 with permission.

Citation: Andersson D, Hughes D, Roth J. 2011. The Origin of Mutants under Selection: Interactions of Mutation, Growth, and Selection, EcoSal Plus 2011; doi:10.1128/ecosalplus.5.6.6
Permissions and Reprints Request Permissions
Download as Powerpoint

Supplemental Material

No supplementary material available for this content.

This is a required field
Please enter a valid email address
Please check the format of the address you have entered.
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error