Key Points
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The bacterial life cycle includes five phases. Traditionally, the life cycle of bacteria in the laboratory is described as having three phases: lag, exponential and stationary phases. However, when batch cultures are incubated for longer periods of time there are two additional phases: death phase and long-term stationary phase.
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During long-term stationary phase, cells expressing the growth advantage in stationary phase (GASP) phenotype emerge. GASP mutations confer a competitive ability to cells during stationary phase.
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The best-characterized GASP mutations are in rpoS. Although mutations in rpoS are not required for expression of the GASP phenotype, mutations that reduce, but do not eliminate, RpoS activity are frequently associated with the expression of GASP.
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Long-term stationary-phase cultures are dynamic. The appearance of GASP mutants reflects the fact that stationary-phase cultures are highly dynamic, with new genotypes constantly appearing over time.
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Mutation frequency can increase during long-term stationary phase. Virtually all long-term batch cultures of Escherichia coli express the GASP phenotype. Furthermore, molecular and genetic methods have shown a wide variety of mutations throughout the chromosome during stationary phase, indicating that mutation frequency is increased during stationary phase, perhaps as a stress response.
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The methyl-directed mismatch repair system and the error-prone DNA polymerases might have a role in the generation of genetic diversity during stationary phase. Data from various experiments indicate that the modulation of the activity of these two systems can help the cell to regulate the degree of fidelity of replication and repair. Under conditions in which the cell senses significant stress, this alteration of mutation frequency can be viewed as a stress response.
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The ability to observe evolution in a test tube in real time might reflect processes that are occurring in natural environments. Incubating bacteria under suboptimal conditions can provide an insight into the stress responses that are active in real-world environments. Unlike the standard incubation protocols in which nutrients are usually in abundance, stationary-phase incubation conditions better simulate the stresses of natural environments. The processes leading to the expression of the GASP phenotype might reflect the mechanisms of generation of genetic diversity used by a wide variety of organisms.
Abstract
The traditional view of the stationary phase of the bacterial life cycle, obtained using standard laboratory culture practices, although useful, might not always provide us with the complete picture. Here, the traditional three phases of the bacterial life cycle are expanded to include two additional phases: death phase and long-term stationary phase. In many natural environments, bacteria probably exist in conditions more akin to those of long-term stationary-phase cultures, in which the expression of a wide variety of stress-response genes and alternative metabolic pathways is essential for survival. Furthermore, stressful environments can result in selection for mutants that express the growth advantage in stationary phase (GASP) phenotype.
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References
Morita, R. Y. Bioavailability of energy and its relationship to growth and starvation in nature. Can. J. Microbiol. 34, 436–441 (1988).
Morita, R. Y. in Starvation in Bacteria (ed. Kjelleberg, S.) 1–23 (Plenum Press, New York, 1988).
Houghton, R. A. The contemporary carbon cycle. In Treatise on Geochemistry Vol. 8 (ed. Schlesinger, W. H.) 473–513 (Elsevier, Amsterdam, 2004).
Gay, F. P. Bacteria growth and reproduction. In Agents of Disease and Host Resistance, Including Principles of Immunology, Bacteriology, Mycology, Protozoology, Parasitology, and Virus Disease (eds Gay, F. P, Bachman, G. W., Benham, R. H. & Buchbinder, L.) 1–38 (Charles C. Thomas, Springfield, 1935).
Finkel, S. E. & Kolter, R. Evolution of microbial diversity during prolonged starvation. Proc. Natl Acad. Sci. USA 96, 4023–4027 (1999). Provided a direct demonstration of the dynamic nature of long-term stationary-phase batch cultures.
Finkel, S. E., Zinser, E. & Kolter, R. in Bacterial Stress Responses (eds Storz, G. & Hengge-Aronis, R.) 231–238 (ASM Press, Washington DC, 2000).
Zambrano, M. M. & Kolter, R. GASPing for life in stationary phase. Cell 86, 181–184 (1996).
Zambrano, M. M., Siegele, D. A., Almirón, M., Tormo, A. & Kolter, R. Microbial competition: E. coli mutants that take over stationary phase cultures. Science 259, 1757–1760 (1993). First description of the appearance of GASP mutants in 10-day-old stationary-phase cultures.
Nystrom, T. Conditional senescence in bacteria: death of the immortals. Mol. Microbiol. 48, 17–23 (2003).
Finkel, S. E. & Kolter, R. DNA as a nutrient: novel role for bacterial competence gene homologs. J. Bacteriol. 183, 6288–6293 (2001).
Jensen, R. B. & Gerdes, K. Programmed cell death in bacteria: proteic plasmid stabilization systems. Mol. Microbiol. 17, 205–210 (1995).
Lehnherr, M., Maguin, E., Jafri, S. & Yarmolinsky, M. B. Plasmid addiction genes of bacteriophage P1: doc, which causes cell death on curing of phage, and phd, which prevents host death when prophage is retained. J. Mol. Biol. 233, 414–428 (1993).
Hayes, F. Toxins–antitoxins: plasmid maintenance, programmed cell death, and cell cycle arrest. Science 301, 1496–1499 (2003).
Brown, J. M. & Shaw, K. J. A novel family of Escherichia coli toxin–antidote gene pairs. J. Bacteriol. 185, 6600–6608 (2003).
Aizenmann, E., Engelberg-Kulka, H. & Glaser, G. An Escherichia coli chromosomal “additional module” regulated by guanosine 3′5′-bispyrophosphate: a model for programmed bacterial cell death. Proc. Natl Acad. Sci. USA 93, 6059–6063 (1996).
Gotfredsen, M. & Gerdes, K. The Escherichia coli relBE genes belong to a new toxin–antitoxin gene family. Mol. Microbiol. 29, 1065–1076.
Christensen, S. K. et al. Overproduction of the Lon protease triggers inhibition of translation in Escherichia coli: involvement of the yefM–yoeB toxin–antitoxin system. Mol. Microbiol. 51, 1705–1717 (2004).
Gerdes, K., Christensen, S. K. & Lobner-Olsen, A. Prokaryotic toxin–antitoxin stress response loci. Nature Rev. Microbiol. 3, 371–382 (2005). Excellent review of the role of toxin–antitoxin pairs.
Steinhaus, E. A. & Birkeland, J. M. Studies on the life and death of bacteria. I. The senescent phase in aging cultures and the probable mechanisms involved. J. Bacteriol. 38, 249–261 (1939). An early paper demonstrating the ability of several bacteria to survive long periods of stationary-phase incubation.
Zinser, E. R. & Kolter, R. K. E. coli evolution during stationary phase. Res. Microbiol. 155, 328–336 (2004). Excellent review of the molecular characterization of several GASP mutants of E. coli.
Zinser, E. R. & Kolter, R. Mutations enhancing amino acid catabolism confer a growth advantage in stationary phase. J. Bacteriol. 181, 5800–5807 (1999).
Zinser, E. R. & Kolter, R. Prolonged stationary phase incubation selects for lrp mutants in E. coli K-12. J. Bacteriol. 182, 4361–4365 (2000).
Zinser, E. R., Schneider, D., Blot, M. & Kolter, R. Bacterial evolution through the selective loss of beneficial genes: trade-offs in expression involving two loci. Genetics 164, 1271–1277 (2003).
Gupta, S. Mutations That Confer a Competitive Advantage During Starvation. Thesis, Harvard Univ. (1997).
Jordan, S. J., Dodd, C. E. & Stewart, G. S. Use of single-strand conformation polymorphism analysis to examine the variability of the rpoS sequence of environmental isolates of salmonellae. Appl. Environ. Microbiol. 65, 3582–3587 (1999).
Farrell, M. J. & Finkel, S. E. The growth advantage in stationary phase phenotype conferred by rpoS mutations is dependent on the pH and nutrient environment. J. Bacteriol. 185, 7044–7052 (2003). Demonstrates the wide diversity of GASP alleles of rpoS in stationary-phase populations.
Bohannon, D. E. et al. Stationary phase-inducible “gearbox” promoters: differential effects of katF mutations and role of σ70. J. Bacteriol. 173, 4482–4492 (1991).
Vijayakumar, S. R. V., Kirchhof, M. G., Patten, C. L. & Schellhorn, H. E. RpoS-regulated genes of Escherichia coli identified by random lacZ fusion mutagenesis. J. Bacteriol. 186, 8499–8507 (2004).
Patten, C. L., Kirchhof, M. G., Schertzberg, M. R., Morton, R. A. & Schellhorn, H. E. Microarray analysis of RpoS-mediated gene expression in Escherichia coli K-12. Mol. Gen. Genomics 272, 580–591 (2004).
Nystrom, T. Growth versus maintenance: a trade-off dicated by RNA polymerase availability and s factor competition. Mol. Microbiol. 54, 855–862 (2004).
Notley-McRobb, L., King, T. & Ferenci, T. rpoS mutations and loss of general stress resistance in Escherichia coli populations as a consequence of conflict between competing stress responses. J. Bacteriol. 184, 806–811 (2002).
Richard, H. T. & Foster, J. W. Acid resistance in Escherichia coli. Adv. Appl. Microbiol. 52, 167–186 (2003).
Vulic, M. & Kolter, R. Evolutionary cheating in E. coli stationary phase cultures. Genetics 158, 519–526 (2001).
Vulic, M. & Kolter, R. Alcohol-induced delay of viability loss in stationary-phase cultures of Escherichia coli. J. Bacteriol. 184, 2898–2905 (2002).
Chen, G., Patten, C. L. & Schellhorn, H. E. Positive selection for loss of RpoS function in Escherichia coli. Mutat. Res. 554, 193–203 (2004).
Krogfelt, K. A., Hjulgaard, M., Sorensen, K., Cohen, P. S. & Givskov, M. rpoS gene function is a disadvantage for Escherichia coli BJ4 during competitive colonization of the mouse large intestine. Infect. Immun. 68, 2518–2524 (2000).
Ferenci, T. What is driving the acquisition of mutS and rpoS polymorphisms in Escherichia coli? Trends Microbiol. 11, 457–461 (2003). Excellent review of the selective pressures that drive mutation in rpoS in nutrient-limited environments.
Notley-McRobb, L. & Ferenci, T. Experimental analysis of molecular events during mutational periodic selections in bacterial evolution. Genetics 156, 1493–1501 (2000).
Finkel, S. E., Zinser, E. R., Gupta, S. & Kolter, R. Life and death in stationary phase. In Molecular Microbiology Vol. H 103 (eds Busby, S. J. W., Thomas, C. M. & Brown, N. L.) 3–16 (Springer-Verlag, Berlin, 1998).
Yeiser, B, Pepper, E. D., Goodman, M. F. & Finkel, S. E. SOS-induced DNA polymerases enhance long-term survival and evolutionary fitness. Proc. Natl Acad. Sci. USA 99, 8737–8741 (2002).
Drake, J. W. A constant rate of spontaneous mutation in DNA-based microbes. Proc. Natl Acad. Sci. USA 88, 7160–7164 (1991).
Drake, J. W., Charlesworth, B., Charlesworth, D. & Crow, J. F. Rates of spontaneous mutation. Genetics 148, 1667–1686 (1998).
Bridges, B. A. Hypermutation in bacteria and other cellular systems. Phil. Trans. R. Soc. Lond. B Biol. Sci. 356, 29–36 (2001).
Torkelson, J. et al. Genome-wide hypermutation in a subpopulation of stationary-phase cells underlies recombination-dependent adaptive mutation. EMBO J. 16, 3303–3311 (1997).
Schofield, M. J. & Hsieh, P. DNA mismatch repair: molecular mechanisms and biological function. Annu. Rev. Microbiol. 57, 579–608 (2003).
Bhagwat, A. S. & Lieb, M. Cooperation and competition in mismatch repair: very short-patch repair and methyl-directed mismatch repair in Escherichia coli. Mol. Microbiol. 44, 1421–1428 (2002).
Macintyre, G., Pitsikas, P. & Cupples, C. G. Growth phase-dependent regulation of Vsr endonuclease may contribute to 5-methylcytosine mutational hot spots in Escherichia coli. J. Bacteriol. 181, 4435–4436 (1999).
Au, K. G, Welsh, K. & Modrich, P. Initiation of methyl-directed mismatch repair. J. Biol. Chem. 267, 12142–12148 (1992).
Herman, G. E. & Modrich, P. Escherichia coli K-12 clones that overproduce dam methylase are hypermutable. J. Bacteriol. 145, 644–646 (1981).
Harris, R. S., et al. Mismatch repair is diminished during stationary phase mutation. Mutat. Res. 437, 51–60 (1999).
Harris, R. S. et al. Mismatch repair protein MutL becomes limiting during stationary-phase mutation. Genes Dev. 11, 2426–2437 (1997).
Zhao, J. & Winkler, M. E. Reduction of GC→TA transversion mutation by overexpression of MutS in Escherichia coli K-12. J. Bacteriol. 182, 5025–5028 (2000).
Bjedov, I. et al. Stress-induced mutagensis in bacteria. Science 300, 1404–1409 (2003).
Akerlund, T., Nordstrom, K. & Bernander, R. Analysis of cell size and DNA content in exponentially growing and stationary phase batch cultures of Escherichia coli. J. Bacteriol. 177, 6791–6797 (1995). Demonstrates that long-term stationary-phase cells frequently have two, four and even eight chromosomes per cell.
Goodman, M. F. Error-prone repair DNA polymerases in prokaryotes and eukaryotes. Annu. Rev. Biochem. 71, 17–50 (2002).
Trobner, W. & Piechocki, R. Competition between isogenic mutS and mut+ populations of Escherichia coli K-12 in continuously growing cultures. Mol. Gen. Genet. 198, 175–176 (1984).
Chao, L. and Cox, E. C. Competition between high and low mutating strains of Escherichia coli. Evolution 15, 931–942 (1998).
Cox, E. C. & Gibson, T. C. Selection of high mutation rates in chemostats. Genetics 77, 169–184 (1974).
Nestmann, E. R. & Hill, R. F. Mutagenesis by mutator gene mutH1 in continuous cultures of Escherichia coli. J. Bacteriol. 119, 33–35 (1974).
Sniegowski, P. D., Gerrish, P. J. & Lenski, R. E. Evolution of high mutation rates in experimental populations of E. coli. Nature 387, 703–705 (1997).
Shaver, A. C. et al. Fitness evolution and the rise of mutator alleles in experimental Escherichia coli populations. Genetics 162, 557–566 (2002).
Sniegowski, P. Evolution: bacterial mutation in stationary phase. Curr. Biol. 14, R245–R246 (2004).
Tegova, R., Tover, A., Tarassova, K., Tark, M. & Kivisaar, M. Involvement of error-prone DNA polymerase IV in stationary-phase mutagenesis in Pseudomonas putida. J. Bacteriol. 186, 2735–2744 (2004).
Wolff, E., Kim, M., Hu, K., Yang, H. & Miller, J. H. Polymerases leave fingerprints: analysis of the mutational spectrum in Escherichia coli rpoB to assess the role of polymerase IV in spontaneous mutation. J. Bacteriol. 186, 2900–2905 (2004).
Rattray, A. J & Strathern, J. N. Error-prone DNA polymerases: when making a mistake is the only way to get ahead. Annu. Rev. Genet. 37, 31–66 (2003).
Tippin, B., Pham, P. & Goodman, M. F. Error-prone replication for better or worse. Trends Microbiol. 12, 288–295 (2004).
Foster, P. L. Stress responses and genetic variation in bacteria. Mutation Res. 569, 3–11 (2005).
Layton, J. C. & Foster, P. L. Error-prone DNA polymerase IV is controlled by the stress-response σ factor, RpoS, in Escherichia coli. Mol. Microbiol. 50, 549–561 (2003). Demonstrated that PolIV is under the control of RpoS during stationary phase.
Matic, I., Taddei, F. & Radman, M. Survival versus maintenance of genetic stability: a conflict of priorities during stress. Res. Microbiol. 155, 337–341 (2004).
Kivisaar, M. Stationary phase mutagenesis: mechanisms that accelerate adaptation of microbial populations under environmental stress. Environ. Microbiol. 5, 814–827 (2003).
LeClerc, J. E., Li, B., Payne, W. L. & Cebula, T. A. High mutation frequencies among Escherichia coli and Salmonella pathogens. Science 274, 1208–1211 (1996).
Kotewicz, M. L. et al. Evolution of multi-gene segments in the mutS–rpoS intergenic region of Salmonella enterica serovar Typhimurium LT2. Microbiology 148, 2531–2540 (2002).
Li, B. et al. Molecular analysis of mutS expression and mutation in natural isolates of pathogenic Escherichia coli. Microbiology 149, 1323–1331 (2003).
Albertini, A. M., Hofer, M., Calos, M. P., Tlsty, T. D. & Miller, J. H. Analysis of spontaneous deletions and gene amplification in the lac region of E. coli. Cold Spring Harb. Symp. Quant. Biol. 47, 841–850 (1983).
Andersson, D. I., Slechta, E. S. & Roth, J. R. Evidence that gene amplification underlies adaptive mutability of the bacterial lac operon. Science 282, 1133–1135 (1998).
Hendrickson, H., Slechta, E. S., Bergthorsson, U., Andersson, D. I. & Roth, J. R. Amplification-mutagenesis: evidence that “directed” adaptive mutation and general hypermutability result from growth with a selected gene amplification. Proc. Natl Acad. Sci. USA 99, 2164–2169 (2002).
Tlsty, T. D., Albertini, A. M. & Miller, J. H. Gene amplifications in the lac region of E. coli. Cell 37, 217–224 (1984).
Whoriskey, S. K., Nghiem, V. H., Leong, P. M., Masson, J. M. & Miller, J. H. Genetic rearrangements and gene amplification in E. coli: DNA sequences at the junctures of amplified gene fusions. Genes Dev. 1, 227–237 (1987).
Anderson, R. P. & Roth, J. R. Tandem genetic duplications in phage and bacteria. Annu. Rev. Microbiol. 31, 473–505 (1977).
Sonti, R. V. & Roth, J. Role of gene duplications in the adaptation of Salmonella typhimurium to growth on limiting carbon sources. Genetics 123, 19–28 (1989).
Petit, M.-A., Dimpfl, J., Radman, M. & Echols, H. Control of large chromosomal duplications in Escherichia coli by the mismatch repair system. Genetics 129, 327–332 (1991).
Porwollik, S. et al. DNA amplification and rearrangements in archival Salmonella enterica serovar typhimurium LT2 cultures. J. Bacteriol. 186, 1678–1682 (2004). Describes significant genomic changes, including deletions and duplications, in long-term stab cultures of Salmonella.
Kudva, I. T. et al. Strains of Escherichia coli O157:H7 differ primarily by insertions or deletions, no single-nucleotide polymorphisms. J. Bacteriol. 184, 1873–1879 (2002).
Welch, R. A. et al. Extensive mosaic structure revealed by the complete genome sequence of uropathogenic Escherichia coli. Proc. Natl Acad. Sci. USA 99, 17020–17024 (2002). A three-way genomic comparison of fully sequenced E. coli strains shows that only ∼40% of genes are shared.
Grozdanov, L. et al. Analysis of the genome structure of the nonpathogenic probiotic Escherichia coli strain Nissle 1917. J. Bacteriol. 186, 5432–5441 (2004).
Schneider, D. et al. Genomic comparisons among Escherichia coli strains B, K-12, and O157:H7 using IS elements as molecular markers. BMC Microbiol. 2, 18 (2002).
Blattner, F. R. et al. The complete genome sequence of Escherichia coli K-12. Science 277, 1453–1474 (1997).
Treves, D. S., Manning, S. & Adams, J. Repeated evolution of an acetate-crossfeeding polymorphism in long-term populations of Escherichia coli. Mol. Biol. Evol. 15, 789–797 (1998).
Adams, J. Microbial evolution in laboratory environments. Res. Microbiol. 155, 311–318 (2004).
Dykhuisen, D. E. Experimental studies of natural selection in bacteria. Annu. Rev. Ecol. Syst. 21, 373–398 (1990).
Guttman D. S. & Dykhuisen, D. E. Clonal divergence in E. coli as a result of recombination, not mutation. Science 266, 1380–1383 (1994).
Cooper, T. E., Rozen, D. E. & Lenski, R. E. Parallel changes in gene expression after 20,000 generations of evolution in E. coli. Proc. Natl Acad. Sci. USA 100, 1072–1077 (2003).
Vasi, F. K. & Lenski, R. E. Ecological strategies and fitness tradeoffs in E. coli mutants adapted to prolonged starvation. J. Genet. 78, 43–39 (1999).
Elena, S. F. & Lenski, R. E. Evolution experiments with microorganisms: the dynamics and genetic bases of adaptation. Nature Rev. Genet. 4, 457–469 (2003).
Lenski, R. E. et al. Evolution of competitive fitness in experimental populations of E. coli: what makes one genotype a better competitor than another? Antonie van Leeuwenhoek 73, 35–47 (1998).
Schneider, D. & Lenski, R. E. Dynamics of insertion sequence elements during experimental evolution of bacteria. Res. Microbiol. 155, 319–327 (2004).
Faure, D. et al. Genomic changes arising in long-term stab cultures of Escherichia coli. J. Bacteriol. 186, 6437–6442 (2004).
Naas, T., Blot, M., Fitch, W. M. & Arber, W. Insertion sequence-related genetic variation in resting Escherichia coli K-12. Genetics 136, 721–730 (1994).
Edwards, K., Linetsky, I. Hueser, C. & Eisenstark, A. Genetic variability among archival cultures of Salmonella typhimurium. FEMS Microbiol. Lett. 199, 215–219 (2001).
Sutton, A., Buencamino, R. & Eisenstark, A. rpoS mutants in archival cultures of Salmonella enterica serovar Typhimurium. J. Bacteriol. 182, 4375–4379 (2000).
Tracy, B. S., Edwards, K. K. & Eisenstark, A. Carbon and nitrogen substrate utilization by archival Salmonella typhimurium LT2 cells. BMC Evol. Biol. 2, 14 (2002).
Acknowledgements
The author is greatly indebted to R. Kolter, in whose laboratory his studies of long-term stationary phase were initiated, to S. Nair, G. O'Toole, V. Palchevskiy, E. Pepper, E. Zinser and three anonymous reviews for helpful comments and discussions, and to K. Sivaraman for assistance in the preparation of the manuscript. Work in the author's laboratory is supported in part by a grant from the W. M. Keck Foundation and a National Science Foundation CAREER award.
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Glossary
- Batch culture
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A closed culture system in which all of the nutrient substrate is added at the beginning.
- Quorum sensing
-
A system by which bacteria communicate. Signalling molecules — chemicals similar to pheromones that are produced by an individual bacterium — can affect the behaviour of surrounding bacteria.
- Toxin–antitoxin
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Paired loci found in the chromosomes of almost all free-living prokaryotes, and many plasmids and phage genomes, encoding a toxin and its antidote that have been proposed to function in bacterial programmed cell death or stress physiology.
- Serial passage
-
An experimental evolution culture system in which a fraction of a culture is sampled and inoculated into a fresh culture of the same medium repeatedly. Over time, cells propagated in this way will show changes in genotype and phenotype associated with changes in relative fitness.
- Alternative sigma (σ) factor
-
Alternative σ factors are produced under specific conditions and allow the RNA polymerase to transcribe a different set of genes than the housekeeping σ factor, σ70.
- Transition
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A mutation between two pyrimidines (T–C) or two purines (A–G).
- Transversion
-
A point mutation in which a purine base is substituted for a pyrimidine base and vice versa; for example, an AT to CG transversion.
- Chemostat
-
A device that allows the continuous growth of a bacterial population on a growth-rate-limiting resource. The resource flows into the chemostat at a constant rate; depleted medium and cells are washed out at the same rate. The population grows and consumes the resource until the bacteria reach an equilibrium density at which their growth rate equals the flow rate through the vessel.
- Very short patch repair
-
A mismatch-correction system that corrects T:G mismatches to C:G in certain sequence contexts, independent of Dam methylation.
- SOS response
-
The bacterial response to DNA damage that is regulated by the LexA and RecA proteins and involves the expression of a network of >40 genes, including several DNA-repair enzymes.
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Finkel, S. Long-term survival during stationary phase: evolution and the GASP phenotype. Nat Rev Microbiol 4, 113–120 (2006). https://doi.org/10.1038/nrmicro1340
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DOI: https://doi.org/10.1038/nrmicro1340
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