Publications

@article{Schneider2000b,

title = {The population genetics of ecological specialization in evolving \textit{Escherichia coli} populations},

author = {Vaughn S. Cooper and Richard E. Lenski},

url = {http://www.nature.com/articles/35037572},

doi = {10.1038/35037572},

issn = {0028-0836},

year  = {2000},

date = {2000-10-01},

urldate = {2000-10-01},

journal = {Nature},

volume = {407},

number = {6805},

pages = {736--739},

abstract = {When organisms adapt genetically to one environment, they may lose fitness in other environments. Two distinct population genetic processes can produce ecological specialization—mutation accumulation and antagonistic pleiotropy. In mutation accumulation, mutations become fixed by genetic drift in genes that are not maintained by selection; adaptation to one environment and loss of adaptation to another are caused by different mutations. Antagonistic pleiotropy arises from trade-offs, such that the same mutations that are beneficial in one environment are detrimental in another. In general, it is difficult to distinguish between these processes. We analysed the decay of unused catabolic functions in 12 lines of \textit{Escherichia coli} propagated on glucose for 20,000 generations. During that time, several lines evolved high mutation rates. If mutation accumulation is important, their unused functions should decay more than the other lines, but no significant difference was observed. Moreover, most catabolic losses occurred early in the experiment when beneficial mutations were being rapidly fixed, a pattern predicted by antagonistic pleiotropy. Thus, antagonistic pleiotropy appears more important than mutation accumulation for the decay of unused catabolic functions in these populations.},

keywords = {Correlated Responses, Fitness Trajectories, Mutation Rates},

pubstate = {published},

tppubtype = {article}

}

@article{Moore2000,

title = {Pervasive compensatory adaptation in \textit{Escherichia coli}},

author = {Francisco B. G. Moore and Daniel E. Rozen and Richard E. Lenski},

url = {https://royalsocietypublishing.org/doi/10.1098/rspb.2000.1030},

doi = {10.1098/rspb.2000.1030},

issn = {0962-8452},

year  = {2000},

date = {2000-03-01},

urldate = {2000-03-01},

journal = {Proceedings of the Royal Society of London. Series B: Biological Sciences},

volume = {267},

number = {1442},

pages = {515--522},

abstract = {To investigate compensatory adaptation (CA), we used genotypes of \textit{Escherichia coli} which were identical except for one or two deleterious mutations. We compared CA for (i) deleterious mutations with large versus small effects, (ii) genotypes carrying one versus two mutations, and (iii) pairs of deleterious mutations which interact in a multiplicative versus synergistic fashion. In all, we studied 14 different genotypes, plus a control strain which was not mutated. Most genotypes showed CA during 200 generations of experimental evolution, where we define CA as a fitness increase which is disproportionately large relative to that in evolving control lines, coupled with retention of the original deleterious mutation(s). We observed greater CA for mutations of large effect than for those of small effect, which can be explained by the greater benefit to recovery in severely handicapped genotypes given the dynamics of selection. The rates of CA were similar for double and single mutants whose initial fitnesses were approximately equal. CA was faster for synergistic than for multiplicative pairs, presumably because the marginal gain which results from CA for one of the component mutations is greater in that case. The most surprising result in our view, is that compensation should be so readily achieved in an organism which is haploid and has little genetic redundancy. This finding suggests a degree of versatility in the \textit{E. coli} genome which demands further study from both genetic and physiological perspectives.},

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}

@article{Rozen2000,

title = {Long-term experimental evolution in \textit{Escherichia coli}. VIII. Dynamics of a balanced polymorphism},

author = {Daniel E. Rozen and Richard E. Lenski},

url = {https://www.journals.uchicago.edu/doi/full/10.1086/303299},

doi = {10.1086/303299},

issn = {00030147},

year  = {2000},

date = {2000-01-01},

urldate = {2000-01-01},

journal = {American Naturalist},

volume = {155},

number = {1},

pages = {24--35},

abstract = {We describe the short- and long-term dynamics of a phenotypic polymorphism that arose in a population of \textit{Escherichia coli} while it was serially propagated for almost 20,000 generations in a glucose-limited minimal medium. The two types, designated \textit{L} and \textit{S}, differ conspicuously in the size of the colonies they form on agar plates as well as the size of their individual cells, and these differences are heritable. The \textit{S} type reached a detectable frequency (>1%) at generation 6,000, and it remained above that frequency throughout the subsequent generations. In addition to morphological differences, \textit{L} and \textit{S} diverged in important ecological properties. With clones isolated at 18,000 generations, \textit{L} has a maximal growth rate in fresh medium that is ~20% higher than that of \textit{S}. However, experiments with conditioned media demonstrate that \textit{L} and \textit{S} secrete one or more metabolites that promote the growth of \textit{S} but not of \textit{L}. The death rate of \textit{L} during stationary phase also increases when \textit{S} is abundant, which suggests that \textit{S} may either secrete a metabolite that is toxic to \textit{L} or remove some factor that enables the survival of \textit{L}. One-day competition experiments with the clones isolated at generation 18,000 show that their relative fitness is frequency dependent, with each type having an advantage when rare. When these two types are grown together for a period of several weeks, they converge on an equilibrium frequency that is consistent with the 1-d competition experiments. Over the entire 14,000-generation period of coexistence, however, the frequency of the \textit{S} type fluctuated between approximately 10% and 85%. We offer several hypotheses that may explain the fluctuations in this balanced polymorphism, including the possibility of coevolution between the two types.},

keywords = {Demography and Ecology},

pubstate = {published},

tppubtype = {article}

}

@article{Vulic1999,

title = {Mutation, recombination, and incipient speciation of bacteria in the laboratory},

author = {M. Vulic and Richard E. Lenski and Miroslav Radman},

url = {http://www.pnas.org/cgi/doi/10.1073/pnas.96.13.7348},

doi = {10.1073/pnas.96.13.7348},

issn = {0027-8424},

year  = {1999},

date = {1999-06-01},

urldate = {1999-06-01},

journal = {Proceedings of the National Academy of Sciences},

volume = {96},

number = {13},

pages = {7348--7351},

abstract = {Mutations in the DNA mismatch repair system increase mutation and recombination. They may thereby promote the genetic divergence that underlies speciation, after which the reacquisition of a functional repair system may sustain that divergence by creating a barrier to recombination. We tested several lines of \textit{Escherichia coli}, derived from a common ancestor and evolved for 20,000 generations, for their recombination ability. Some lines, but not others, had become mismatch repair-defective mutators during experimental evolution, providing different opportunities for DNA sequence divergence. We knocked out the repair system in lines that had retained this function, and we restored function to those lines that had become defective. We then estimated recombination rates in various crosses between these repair- deficient and -proficient strains. The effect of the mismatch repair system on recombination was greatest in those lines that had evolved nonfunctional repair, indicating they had undergone more sequence divergence and, consequently, were more sensitive to the recombination-inhibiting effect of a functional repair system. These results demonstrate the establishment of an incipient genetic barrier between formerly identical lines, and they support a model in which the mismatch repair system can influence speciation dynamics through its simultaneous effects on mutation and recombination.},

keywords = {Genome Evolution, Mutation Rates},

pubstate = {published},

tppubtype = {article}

}

@article{Vasi1999,

title = {Ecological strategies and fitness tradeoffs in \textit{Escherichia coli} mutants adapted to prolonged starvation},

author = {Farida K. Vasi and Richard E. Lenski},

url = {http://link.springer.com/10.1007/BF02994702},

doi = {10.1007/BF02994702},

issn = {0022-1333},

year  = {1999},

date = {1999-04-01},

urldate = {1999-04-01},

journal = {Journal of Genetics},

volume = {78},

number = {1},

pages = {43--49},

abstract = {Many bacteria in nature are nutritionally deprived, and there has been heightened interest during the past decade in the properties of these bacteria. We subjected five populations of \textit{Escherichia coli} to prolonged starvation in a minimal salts medium, during which time the density of viable cells declined by several orders of magnitude. From each one, we isolated a surviving clone that showed some heritable difference in colony morphology. We then characterized these mutants in two ecologically relevant respects. First, we determined the nature of their selective advantage, if any, during prolonged starvation. (i) Three of the five mutants had significantly lower net death rate when progenitor and mutant clones were starved separately. (ii) Three mutants showed a significant reduction in death rate in mixed culture that was frequency dependent and manifest when the mutant clone was initially rare. This pattern suggests that these mutants fed on some byproduct of progenitor cells (living or dead). (iii) Two mutants caused the death rate of their progenitors to increase significantly relative to the rate measured in the absence of the mutant. This pattern suggests that these mutants had become allelopathic to their progenitors. Thus, three distinct ecological adaptations to prolonged starvation are evident. No advantage was detected for one mutant, whereas two mutants exhibited multiple advantages. Second, we asked whether the starvation-selected mutants were as fit in growth-supporting conditions as their progenitors. All five mutants were inferior to their progenitor during competition in fresh medium. Evidently, there is an evolutionary tradeoff between performance under growth and starvation conditions. },

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}

@article{Mongold1999,

title = {Evolutionary adaptation to temperature. VII. Extension of the upper thermal limit of \textit{Escherichia coli}},

author = {Judith A. Mongold and Albert F. Bennett and Richard E. Lenski},

url = {https://onlinelibrary.wiley.com/doi/10.1111/j.1558-5646.1999.tb03774.x},

doi = {10.1111/j.1558-5646.1999.tb03774.x},

issn = {0014-3820},

year  = {1999},

date = {1999-04-01},

urldate = {1999-04-01},

journal = {Evolution},

volume = {53},

number = {2},

pages = {386--394},

abstract = {What factors influence the ability of populations to adapt to extreme environments that lie outside their current tolerance limits? We investigated this question by exposing experimental populations of the bacterium \textit{Escherichia coli} to lethally high temperatures. We asked: (1) whether we could obtain thermotolerant mutants with an extended upper thermal limit by this selective screen; (2) whether the propensity to obtain thermotolerant mutants depended on the prior selective history of the progenitor genotypes; and (3) how the fitness properties of these mutants compared to those of their progenitors within the ancestral thermal niche. Specifically, we subjected 15 independent populations founded from each of six progenitors to 44°C; all of the progenitors had upper thermal limits between about 40°C and 42°C. Two of the progenitors were from populations that had previously adapted to 32°C, two were from populations adapted to 37°C, and two were from populations adapted to 41-42°C. All 90 populations were screened for mutants that could survive and grow at 44°C. We obtained three thermotolerant mutants, all derived from progenitors previously adapted to 41-42°C. In an earlier study, we serendipitously found one other thermotolerant mutant derived from a population that had previously adapted to 32°C. Thus, prior selection at an elevated but nonlethal temperature may predispose organisms to evolve more extreme thermotolerance, but this is not an absolute requirement. It is evidently possible to obtain mutants that tolerate more extreme temperatures, so why did they not become prevalent during prior selection at 41-42°C, near the upper limit of the thermal niche? To address this question, we measured the fitness of the thermotolerant mutants at high temperatures just within the ancestral niche. None of the four thermotolerant mutants had an advantage relative to their progenitor even very near the upper limit of the thermal niche; in fact, all of the mutants showed a noticeable loss of fitness around 41°C. Thus, the genetic adaptations that improve competitive fitness at high but nonlethal temperatures are distinct from those that permit tolerance of otherwise lethal temperatures.},

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}

@article{10.1093/icb/39.2.346,

title = {Experimental Evolution and Its Role in Evolutionary Physiology},

author = {Albert F. Bennett and Richard E. Lenski},

url = {https://doi.org/10.1093/icb/39.2.346 

https://academic.oup.com/icb/article-lookup/doi/10.1093/icb/39.2.346},

doi = {10.1093/icb/39.2.346},

issn = {0003-1569},

year  = {1999},

date = {1999-04-01},

urldate = {1999-04-01},

journal = {American Zoologist},

volume = {39},

number = {2},

pages = {346--362},

abstract = {Four general approaches to the study of evolutionary physiology—phylogenetically-based comparisons, genetic analyses and manipulations, phenotypic plasticity and manipulation, and selection studies—are outlined and discussed. We provide an example of the latter, the application of laboratory selection experiments to the study of a general issue in environmental adaptation, differences in adaptive patterns of generalists and specialists. A clone of the bacterium \textit{Escherichia coli} that had evolved in a constant environment of 37°C was replicated into 6 populations and allowed to reproduce for 2,000 generations in a variable thermal environment alternating between 32 and 42°C. As predicted by theory, fitness and efficiency of resource use increased in this new environment, as did stress resistance. Contrary to predictions, however, fitness and efficiency in the constant ancestral environment of 37°C did not decrease, nor did thermal niche breadth or phenotypic plasticity increase. Selection experiments can thus provide a valuable approach to testing hypotheses and assumptions about the evolution of functional characters.},

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Diminishing returns from mutation supply rate in asexual populations.},

author = {J. Arjan G. M. {de Visser} and C. W. Zeyl and Philip J. Gerrish and Jeffrey L. Blanchard and Richard E. Lenski},

url = {https://www.science.org/lookup/doi/10.1126/science.283.5400.404},

doi = {10.1126/science.283.5400.404},

issn = {00368075},

year  = {1999},

date = {1999-01-15},

urldate = {1999-01-15},

journal = {Science},

volume = {283},

pages = {404-406},

abstract = {Mutator genotypes with increased mutation rates may be especially important in microbial evolution if genetic adaptation is generally limited by the supply of mutations. In experimental populations of the bacterium \textit{Escherichia coli}, the rate of evolutionary adaptation was proportional to the mutation supply rate only in particular circumstances of small or initially well-adapted populations. These experiments also demonstrate a "speed limit" on adaptive evolution in asexual populations, one that is independent of the mutation supply rate.},

keywords = {Descendant Experiments, Fitness Trajectories, Mutation Rates},

pubstate = {published},

tppubtype = {article}

}

@article{Papadopoulos3807,

title = {Genomic evolution during a 10,000-generation experiment with bacteria},

author = {Dimitri Papadopoulos and Dominique Schneider and Jessica Meier-Eiss and Werner Arber and Richard E. Lenski and Michel Blot},

url = {https://www.pnas.org/content/96/7/3807},

doi = {10.1073/pnas.96.7.3807},

issn = {0027-8424},

year  = {1999},

date = {1999-01-01},

urldate = {1999-01-01},

journal = {Proceedings of the National Academy of Sciences},

volume = {96},

number = {7},

pages = {3807--3812},

publisher = {National Academy of Sciences},

abstract = {Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of \textit{Escherichia coli} evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations. The evolving genomes became increasingly different from their ancestor over time. Moreover, tremendous diversity accumulated within each population, such that almost every individual had a different genetic fingerprint after 10,000 generations. As has been often suggested, but not previously shown by experiment, the rates of phenotypic and genomic change were discordant, both across replicate populations and over time within a population. Certain pivotal mutations were shared by all descendants in a population, and these are candidates for beneficial mutations, which are rare and difficult to find. More generally, these data show that the genome is highly dynamic even over a time scale that is, from an evolutionary perspective, very brief. },

keywords = {Genome Evolution, Mutation Rates},

pubstate = {published},

tppubtype = {article}

}

@article{Turner1998,

title = {Tradeoff between horizontal and vertical modes of transmission in bacterial plasmids.},

author = {Paul E. Turner and Vaughn S. Cooper and Richard E. Lenski},

url = {https://onlinelibrary.wiley.com/doi/10.1111/j.1558-5646.1998.tb01634.x},

doi = {10.1111/j.1558-5646.1998.tb01634.x},

issn = {0014-3820},

year  = {1998},

date = {1998-04-01},

urldate = {1998-04-01},

journal = {Evolution},

volume = {52},

number = {2},

pages = {315--329},

abstract = {It has been hypothesized that there is a fundamental conflict between horizontal (infectious) and vertical (intergenerational) modes of parasite transmission. Activities of a parasite that increase its rate of infectious transmission are presumed to reduce its host's fitness. This reduction in host fitness impedes vertical transmission of the parasite and causes a tradeoff between horizontal and vertical transmission. Given this tradeoff, and assuming no multiple infections (no within-host competition among parasites), a simple model predicts that the density of uninfected hosts in the environment should determine the optimum balance between modes of parasite transmission. When susceptible hosts are abundant, selection should favor increased rates of horizontal transfer, even at the expense of reduced vertical transmission. Conversely, when hosts are rare, selection should favor increased vertical transmission even at the expense of lower horizontal transfer. We tested the tradeoff hypothesis and these evolutionary predictions using conjugative plasmids and the bacteria that they infect. Plasmids were allowed to evolve for 500 generations in environments with different densities of susceptible hosts. The plasmid's rate of horizontal transfer by conjugation increased at the expense of host fitness, indicating a tradeoff between horizontal and vertical transmission. Also, reductions in conjugation rate repeatedly coincided with the loss of a particular plasmid-encoded antibiotic resistance gene. However, susceptible host density had no significant effect on the evolution of horizontal versus vertical modes of plasmid transmission. We consider several possible explanations for the failure to observe such an effect.},

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}

@article{Lenski1998,

title = {Evolution of competitive fitness in experimental populations of \textit{E. coli}: What makes one genotype a better competitor than another?},

author = {Richard E. Lenski and Judith A. Mongold and Paul D. Sniegowski and Michael Travisano and Farida K. Vasi and Philip J. Gerrish and Thomas M. Schmidt},

url = {https://link.springer.com/article/10.1023%2FA%3A1000675521611},

doi = {10.1023/A:1000675521611},

issn = {00036072},

year  = {1998},

date = {1998-01-01},

urldate = {1998-01-01},

journal = {Antonie van Leeuwenhoek, International Journal of General and Molecular Microbiology},

volume = {73},

number = {1},

pages = {35--47},

abstract = {An important problem in microbial ecology is to identify those phenotypic attributes that are responsible for competitive fitness in a particular environment. Thousands of papers have been published on the physiology, biochemistry, and molecular genetics of \textit{Escherichia coli} and other bacterial models. Nonetheless, little is known about what makes one genotype a better competitor than another even in such well studied systems. Here, we review experiments to identify the phenotypic bases of improved competitive fitness in twelve \textit{E. coli} populations that evolved for thousands of generations in a defined environment, in which glucose was the limiting substrate. After 10,000 generations, the average fitness of the derived genotypes had increased by ~ 50% relative to the ancestor, based on competition experiments using marked strains in the same environment. The growth kinetics of the ancestral and derived genotypes showed that the latter have a shorter lag phase upon transfer into fresh medium and a higher maximum growth rate. Competition experiments were also performed in environments where other substrates were substituted for glucose. The derived genotypes are generally more fit in competition for those substrates that use the same mechanism of transport as glucose, which suggests that enhanced transport was an important target of natural selection in the evolutionary environment. All of the derived genotypes produce much larger cells than does the ancestor, even when both types are forced to grow at the same rate. Some, but not all, of the derived genotypes also have greatly elevated mutation rates. Efforts are now underway to identify the genetic changes that underlie those phenotypic changes, especially substrate specificity and elevated mutation rate, for which there are good candidate loci. Identification and subsequent manipulation of these genes may provide new insights into the reproducibility of adaptive evolution, the importance of co-adapted gene complexes, and the extent to which distinct phenotypes (e.g., substrate specificity and cell size) are affected by the same mutations.},

keywords = {Review Articles},

pubstate = {published},

tppubtype = {article}

}

@article{article,

title = {The fate of competing beneficial mutations in an asexual population},

author = {Philip J. Gerrish and Richard E. Lenski},

url = {https://link.springer.com/article/10.1023%2FA%3A1017067816551},

doi = {10.1023/A:1017067816551},

isbn = {978-94-010-6193-3},

year  = {1998},

date = {1998-01-01},

urldate = {1998-01-01},

journal = {Genetica},

volume = {102-103},

pages = {127-44},

abstract = {In sexual populations, beneficial mutations that occur in different lineages may be recombined into a single lineage. In asexual populations, however, clones that carry such alternative beneficial mutations compete with one another and, thereby, interfere with the expected progression of a given mutation to fixation. From theoretical exploration of such ‘clonal interference’, we have derived (1) a fixation probability for beneficial mutations, (2) an expected substitution rate, (3) an expected coefficient of selection for realized substitutions, (4) an expected rate of fitness increase, (5) the probability that a beneficial mutation transiently achieves polymorphic frequency (≥ 1%), and (6) the probability that a beneficial mutation transiently achieves majority status. Based on (2) and (3), we were able to estimate the beneficial mutation rate and the distribution of mutational effects from changes in mean fitness in an evolving \textit{E. coli} population.},

keywords = {Theory and Simulations},

pubstate = {published},

tppubtype = {article}

}

@article{Elena1998,

title = {Distribution of fitness effects caused by random insertion mutations in \textit{Escherichia coli}.},

author = {Santiago F. Elena and Lynette Ekunwe and Neerja Hajela and Shenandoah A. Oden and Richard E. Lenski},

url = {http://www.ncbi.nlm.nih.gov/pubmed/9720287},

doi = {10.1023/a:1017031008316},

issn = {0016-6707},

year  = {1998},

date = {1998-01-01},

urldate = {1998-01-01},

journal = {Genetica},

volume = {102-103},

number = {1-6},

pages = {349--58},

abstract = {Very little is known about the distribution of mutational effects on organismal fitness, despite the fundamental importance of this information for the study of evolution. This lack of information reflects the fact that it is generally difficult to quantify the dynamic effects of mutation and natural selection using only static distributions of allele frequencies. In this study, we took a direct approach to measuring the effects of mutations on fitness. We used transposon-mutagenesis to create 226 mutant clones of \textit{Escherichia coli}. Each mutant clone carried a single random insertion of a derivative of Tn\textit{10}. All 226 mutants were independently derived from the same progenitor clone, which was obtained from a population that had evolved in a constant laboratory environment for 10,000 generations. We then performed competition experiments to measure the effect of each mutation on fitness relative to a common competitor. At least 80% of the mutations had a significant negative effect on fitness, whereas none of the mutations had a significant positive effect. The mutations reduced fitness by about 3%, on average, but the distribution of fitness effects was highly skewed and had a long, flat tail. A compound distribution, which includes both gamma and uniform components, provided an excellent fit to the observed fitness values.},

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}

@article{Elena1997b,

title = {Test of synergistic interactions among deleterious mutations in bacteria},

author = {Santiago F. Elena and Richard E. Lenski},

url = {http://www.nature.com/articles/37108},

doi = {10.1038/37108},

issn = {0028-0836},

year  = {1997},

date = {1997-11-01},

urldate = {1997-11-01},

journal = {Nature},

volume = {390},

number = {6658},

pages = {395--398},

abstract = {Identifying the forces responsible for the origin and maintenance of sexuality remains one of the greatest unsolved problems in biology. The mutational deterministic hypothesis postulates that sex is an adaptation that allows deleterious mutations to be purged from the genome; it requires synergistic interactions, which means that two mutations would be more harmful together than expected from their separate effects. We generated 225 genotypes of \textit{Escherichia coli} carrying one, two or three successive mutations and measured their fitness relative to an unmutated competitor. The relationship between mutation number and average fitness is nearly log- linear. We also constructed 27 recombinant genotypes having pairs of mutations whose separate and combined effects on fitness were determined. Several pairs exhibit significant interactions for fitness, but they are antagonistic as often as they are synergistic. These results do not support the mutational deterministic hypothesis for the evolution of sex.},

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}

@article{Elena1997,

title = {Long-term experimental evolution in \textit{Escherichia coli}. VII. Mechanisms maintaining genetic variability within populations.},

author = {Santiago F. Elena and Richard E. Lenski},

url = {https://onlinelibrary.wiley.com/doi/10.1111/j.1558-5646.1997.tb03953.x},

doi = {10.1111/j.1558-5646.1997.tb03953.x},

issn = {0014-3820},

year  = {1997},

date = {1997-08-01},

urldate = {1997-08-01},

journal = {Evolution},

volume = {51},

number = {4},

pages = {1058--1067},

abstract = {Six replicate populations of the bacterium \textit{Escherichia coli} were propagated for more than 10,000 generations in a defined environment. We sought to quantify the variation among clones within these populations with respect to their relative fitness, and to evaluate the roles of three distinct population genetic processes in maintaining this variation. On average, a pair of clones from the same population differed from one another in their relative fitness by approximately 4%. This within-population variation was small compared with the average fitness gain relative to the common ancestor, but it was statistically significant. According to one hypothesis. The variation in fitness is transient and reflects the ongoing substitution of beneficial alleles. We used Fisher's fundamental theorem to compare the observed rate of each population's change in mean fitness with the extent of variation for fitness within that population, but we failed to discern any correspondence between these quantities. A second hypothesis supposes that the variation in fitness is maintained by recurrent deleterious mutations that give rise to a mutation-selection balance. To test this hypothesis, we made use of the fact that two of the six replicate populations had evolved mutator phenotypes, which gave them a genomic mutation rate approximately 100-fold higher than that of the other populations. There was a marginally significant correlation between a population's mutation rate and the extent of its within-population variance for fitness, but this correlation was driven by only one population (whereas two of the populations had elevated mutation rates). Under a third hypothesis, this variation is maintained by frequency-dependent selection, whereby genotypes have an advantage when they are rare relative to when they are common. In all six populations, clones were more fit, on average, when they were rare than when they were common, although the magnitude of the advantage when rare was usually small (~1% in five populations and ~45% in the other). These three hypotheses are not mutually exclusive, but frequency-dependent selection appears to be the primary force maintaining the fitness variation within these experimental populations.},

keywords = {Demography and Ecology, Fitness Trajectories, Mutation Rates, Theory and Simulations},

pubstate = {published},

tppubtype = {article}

}

@article{Sniegowski1997,

title = {Evolution of high mutation rates in experimental populations of \textit{E. coli}},

author = {Paul D. Sniegowski and Philip J. Gerrish and Richard E. Lenski},

url = {http://www.nature.com/articles/42701},

doi = {10.1038/42701},

issn = {0028-0836},

year  = {1997},

date = {1997-06-01},

urldate = {1997-06-01},

journal = {Nature},

volume = {387},

number = {6634},

pages = {703--705},

abstract = {Most mutations are likely to be deleterious, and so the spontaneous mutation rate is generally held at a very low value. Nonetheless, evolutionary theory predicts that high mutation rates can evolve under certain circumstances. Empirical observations have previously been limited to short-term studies of the fates of mutator strains deliberately introduced into laboratory populations of \textit{Escherichia coli}, and to the effects of intense selective events on mutator frequencies in \textit{E. coli}. Here we report the rise of spontaneously originated mutators in populations of \textit{E. coli} undergoing long-term adaptation to a new environment. Our results corroborate computer simulations of mutator evolution in adapting clonal populations, and may help to explain observations that associate high mutation rates with emerging pathogens and with certain cancers.},

keywords = {Genotypes and Phenotypes, Mutation Rates},

pubstate = {published},

tppubtype = {article}

}

@article{Bennett1997,

title = {Evolutionary adaptation to temperature. VI. Phenotypic acclimation and its evolution in \textit{Escherichia coli}},

author = {Albert F. Bennett and Richard E. Lenski},

url = {https://onlinelibrary.wiley.com/doi/10.1111/j.1558-5646.1997.tb02386.x},

doi = {10.1111/j.1558-5646.1997.tb02386.x},

issn = {0014-3820},

year  = {1997},

date = {1997-02-01},

urldate = {1997-02-01},

journal = {Evolution},

volume = {51},

number = {1},

pages = {36--44},

abstract = {Acclimation refers to reversible, nongenetic changes in phenotype that are induced by specific environmental conditions. Acclimation is generally assumed to improve function in the environment that induces it (the beneficial acclimation hypothesis). In this study, we experimentally tested this assumption by measuring relative fitness of the bacterium \textit{Escherichia coli} acclimated to different thermal environments. The beneficial acclimation hypothesis predicts that bacteria acclimated to the temperature of competition should have greater fitness than do bacteria acclimated to any other temperature. The benefit predicted by the hypothesis was found in only seven of 12 comparisons; in the other comparisons, either no statistically demonstrable benefit was observed or a detrimental effect of acclimation was demonstrated. For example, in a lineage evolutionarily adapted to 37°C, bacteria acclimated to 37°C have a higher fitness at 32°C than do bacteria acclimated to 32°C, a result exactly contrary to prediction; acclimation to 27°C or 40°C prior to competition at those temperatures confers no benefit over 37°C acclimated forms. Consequently, the beneficial acclimation hypothesis must be rejected as a general prediction of the inevitable result of phenotypic adjustments associated with new environments. However, the hypothesis is supported in many instances when the acclimation and competition temperatures coincide with the historical temperature at which the bacterial populations have evolved. For example, when the evolutionary temperature of the population was 37°C, bacteria acclimated to 37°C had superior fitness at 37°C to those acclimated to 32°C; similarly, bacteria evolutionarily adapted to 32°C had a higher fitness during competition at 32°C than they did when acclimated to 37°C. The more surprising results are that when the bacteria are acclimated to their historical evolutionary temperature, they are frequently competitively superior even at other temperatures. For example, bacteria that have evolved at either 20°C or 32°C and are acclimated to their respective evolutionary temperatures have a greater fitness at 37°C than when they are acclimated to 37°C. Thus, acclimation to evolutionary temperature may, as a correlated consequence, enhance performance not only in the evolutionary environment, but also in a variety of other thermal environments.},

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}

@article{Souza1997,

title = {Long-term experimental evolution in \textit{Escherichia coli}. V. Effects of recombination with immigrant genotypes on the rate of bacterial evolution},

author = {Valeria Souza and Paul E. Turner and Richard E. Lenski},

url = {https://turnerlab.yale.edu/sites/default/files/souza_etal_1997.pdf

https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1420-9101.1997.10050743.x},

doi = {https://doi.org/10.1046/j.1420-9101.1997.10050743.x},

issn = {1010061X},

year  = {1997},

date = {1997-01-01},

urldate = {1997-01-01},

journal = {Journal of Evolutionary Biology},

volume = {10},

number = {5},

pages = {743},

abstract = {This study builds upon an earlier experiment that examined the dynamics of mean fitness in evolving populations of \textit{Escherichia coli} in which mutations were the sole source of genetic variation. During thousands of generations in a constant environment, the rate of improvement in mean fitness of these asexual populations slowed considerably from an initially rapid pace. In this study, we sought to determine whether sexual recombination with novel genotypes would reaccelerate the rate of adaption in these populations. To that end, treatment populations were propagated for an additional 1000 generations in the same environment as their ancestors, but they were periodically allowed to mate with an immigrant pool of genetically distinct Hfr (high frequency recombination) donors. These donors could transfer genes to the resident populations by conjugation, but the donors themselves could not grow in the experimental environment. Control populations were propagated under identical conditions, but in the absence of sexual recombination with the donors. All twelve control populations retained the ancestral alleles at every locus that was scored. In contrast, the sexual recombination treatment yielded dramatic increases in genetic variation. Thus, there was a profound effect of recombination on the rate of genetic change. However, the increased genetic variation in the treatment populations had no significant effect on the rate of adaptive evolution, as measured by changes in mean fitness relative to a common competitor. We then considered three hypotheses that might reconcile these two outcomes: recombination pressure, hitchhiking of recombinant genotypes in association with beneficial mutations, and complex selection dynamics whereby certain genotypes may have a selective advantage only within a particular milieu of competitors. The estimated recombination rate was too low to explain the observed rate of genetic change, either alone or in combination with hitchhiking effects. However, we documented complex ecological interactions among some recombinant genotypes, suggesting that our method for estimating fitness relative to a common competitor might have underestimated the rate of adaptive evolution in the treatment populations.},

keywords = {Descendant Experiments},

pubstate = {published},

tppubtype = {article}

}