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3. Antibiotic resistance alters the ability of Pseudomonas aeruginosa to invade bacteria from the respiratory microbiome.

Author

Lindon, Selina, Shah, Sarah, Gifford, Danna R, Lood, Cédric, Font, Maria A Gomis, Kaur, Divjot, Oliver, Antonio, MacLean, R Craig, and Wheatley, Rachel M

Subjects
DRUG resistance in bacteria, STAPHYLOCOCCUS epidermidis, PSEUDOMONAS aeruginosa, GENETIC mutation, STAPHYLOCOCCUS
Abstract

The emergence and spread of antibiotic resistance in bacterial pathogens is a global health threat. One important unanswered question is how antibiotic resistance influences the ability of a pathogen to invade the host-associated microbiome. Here we investigate how antibiotic resistance impacts the ability of a bacterial pathogen to invade bacteria from the microbiome, using the opportunistic bacterial pathogen Pseudomonas aeruginosa and the respiratory microbiome as our model system. We measure the ability of P. aeruginosa spontaneous antibiotic-resistant mutants to invade pre-established cultures of commensal respiratory microbes in an assay that allows us to link specific resistance mutations with changes in invasion ability. While commensal respiratory microbes tend to provide some degree of resistance to P. aeruginosa invasion, antibiotic resistance is a double-edged sword that can either help or hinder the ability of P. aeruginosa to invade. The directionality of this help or hindrance depends on both P. aeruginosa genotype and respiratory microbe identity. Specific resistance mutations in genes involved in multidrug efflux pump regulation are shown to facilitate the invasion of P. aeruginosa into Staphylococcus lugdunensis , yet impair invasion into Rothia mucilaginosa and Staphylococcus epidermidis. Streptococcus species provide the strongest resistance to P. aeruginosa invasion, and this is maintained regardless of antibiotic resistance genotype. Our study demonstrates how the cost of mutations that provide enhanced antibiotic resistance in P. aeruginosa can crucially depend on community context. We suggest that attempts to manipulate the microbiome should focus on promoting the growth of commensals that can increase the fitness costs associated with antibiotic resistance and provide robust inhibition of both wildtype and antibiotic-resistant pathogen strains. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Population genetics of rifampicin-resistant Pseudomonas aeruginosa

Author

Gifford, Danna R. and MacLean, R. Craig

Subjects
616.9, Biology, Evolution (zoology), experimental evolution
Abstract

Antibiotic resistance is generally associated with a cost in terms of reduced competitive fitness in the absence of antibiotics. Despite this 'cost of resistance', the cessation of antibiotic treatment does not result in significant reductions in the prevalence of resistance. The maintenance of resistance, in spite of the costs, has been attributed to the rarity of reversion mutations, relative to compensatory mutations at other loci in the genome. However, the large size of bacteria populations, and the potential for migration, suggest that reversion mutations should occasionally be introduced to resistant populations. In this thesis, I show that additional mechanisms can prevent fixation of reversion mutations even if they do occur. Using an experimental evolution approach, with rifampicin resistance in Pseudomonas aeruginosa as a model system, I measured the costs of resistance in several environments and followed the adaptive dynamics of resistant populations where a sensitive lineage had invaded by migration. The results suggest that several additional mechanisms contribute to the maintenance of antibiotic resistance. Most rifampicin resistance mutations are not unconditionally costly in all environments, suggesting that migration between environments could maintain a resistant reservoir population. In environments where resistance is initially costly, the fixation of a revertant is not guaranteed, even if introduced through migration. Revertant fixation was impeded or prevented by clonal interference from adaptation in the resistant strain. Revertants that did successfully replace the resistant strain were forced to adapt to do so. Contrary to assumptions in the existing literature, fitness in the resistant strains was not recovered by general compensatory mutations, but instead by adaptive mutations specific to the environment. The data challenge several assumptions about the maintenance of antibiotic resistance: that resistance mutations are always costly, that the rarity of back mutations prevents the reversion of resistance, and that resistant strains recover fitness by compensatory mutations.

Published
2014

8. For the love of fish, nature and people: A tribute to Professor Louis Bernatchez (1960–2023)

Author

Wellenreuther, Maren, primary, Ferchaud, Anne‐Laure, additional, Beheregaray, Luciano B., additional, Bierne, Nicolas, additional, Correa, Alberto Soares, additional, Elmer, Kathryn, additional, Fraser, Dylan, additional, Gifford, Danna, additional, Gompert, Zachariah, additional, Johnson, Marc, additional, Kassen, Rees, additional, Martin, Ryan, additional, Meek, Mariah, additional, Mergeay, Joachim, additional, Mérot, Claire, additional, Naish, Kerry, additional, Narum, Shawn, additional, Sunnucks, Paul, additional, Thomas, Frédéric, additional, Thrall, Peter, additional, Yáñez, José Manuel, additional, Zhan, Jiasui, additional, and Zhan, Xiangjiang, additional

Published
2023
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16. Mutators can drive the evolution of multi-resistance to antibiotics

Author

Gifford, Danna R., Berrios-Caro, Ernesto, Joerres, Christine, Suñé, Marc, Forsyth, Jessica H., Bhattacharyya, Anish, Galla, Tobias, Knight, Christopher G., Gifford, Danna R., Berrios-Caro, Ernesto, Joerres, Christine, Suñé, Marc, Forsyth, Jessica H., Bhattacharyya, Anish, Galla, Tobias, and Knight, Christopher G.

Abstract

Antibiotic combination therapies are an approach used to counter the evolution of resistance; their purported benefit is they can stop the successive emergence of independent resistance mutations in the same genome. Here, we show that bacterial populations with ‘mutators’, organisms with defects in DNA repair, readily evolve resistance to combination antibiotic treatment when there is a delay in reaching inhibitory concentrations of antibiotic—under conditions where purely wild-type populations cannot. In populations of Escherichia coli subjected to combination treatment, we detected a diverse array of acquired mutations, including multiple alleles in the canonical targets of resistance for the two drugs, as well as mutations in multi-drug efflux pumps and genes involved in DNA replication and repair. Unexpectedly, mutators not only allowed multi-resistance to evolve under combination treatment where it was favoured, but also under single-drug treatments. Using simulations, we show that the increase in mutation rate of the two canonical resistance targets is sufficient to permit multi-resistance evolution in both single-drug and combination treatments. Under both conditions, the mutator allele swept to fixation through hitch-hiking with single-drug resistance, enabling subsequent resistance mutations to emerge. Ultimately, our results suggest that mutators may hinder the utility of combination therapy when mutators are present. Additionally, by raising the rates of genetic mutation, selection for multi-resistance may have the unwanted side-effect of increasing the potential to evolve resistance to future antibiotic treatments., QC 20230630

Published
2023
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17. Mutators can drive the evolution of multi-resistance to antibiotics

Author

Biotechnology and Biological Sciences Research Council (UK), UK Research and Innovation, Rutherford Foundation, University of Manchester, Wellcome Trust, Agencia Estatal de Investigación (España), Swedish Research Council, Gifford, Danna R., Berríos-Caro, Ernesto, Joerres, Christine, Suñé, Marc, Forsyth, Jessica H., Bhattacharyya, Anish, Galla, Tobias, Knight, Christopher G., Biotechnology and Biological Sciences Research Council (UK), UK Research and Innovation, Rutherford Foundation, University of Manchester, Wellcome Trust, Agencia Estatal de Investigación (España), Swedish Research Council, Gifford, Danna R., Berríos-Caro, Ernesto, Joerres, Christine, Suñé, Marc, Forsyth, Jessica H., Bhattacharyya, Anish, Galla, Tobias, and Knight, Christopher G.

Abstract

Antibiotic combination therapies are an approach used to counter the evolution of resistance; their purported benefit is they can stop the successive emergence of independent resistance mutations in the same genome. Here, we show that bacterial populations with 'mutators', organisms with defects in DNA repair, readily evolve resistance to combination antibiotic treatment when there is a delay in reaching inhibitory concentrations of antibiotic-under conditions where purely wild-type populations cannot. In populations of Escherichia coli subjected to combination treatment, we detected a diverse array of acquired mutations, including multiple alleles in the canonical targets of resistance for the two drugs, as well as mutations in multi-drug efflux pumps and genes involved in DNA replication and repair. Unexpectedly, mutators not only allowed multi-resistance to evolve under combination treatment where it was favoured, but also under single-drug treatments. Using simulations, we show that the increase in mutation rate of the two canonical resistance targets is sufficient to permit multi-resistance evolution in both single-drug and combination treatments. Under both conditions, the mutator allele swept to fixation through hitch-hiking with single-drug resistance, enabling subsequent resistance mutations to emerge. Ultimately, our results suggest that mutators may hinder the utility of combination therapy when mutators are present. Additionally, by raising the rates of genetic mutation, selection for multi-resistance may have the unwanted side-effect of increasing the potential to evolve resistance to future antibiotic treatments.

Published
2023

26. Competition delays multi-drug resistance evolution during combination therapy

Author

University of Manchester, Wellcome Trust, UK Research and Innovation, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Berríos-Caro, Ernesto, Gifford, Danna R., Galla, Tobias, University of Manchester, Wellcome Trust, UK Research and Innovation, Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Berríos-Caro, Ernesto, Gifford, Danna R., and Galla, Tobias

Abstract

Combination therapies have shown remarkable success in preventing the evolution of resistance to multiple drugs, including HIV, tuberculosis, and cancer. Nevertheless, the rise in drug resistance still remains an important challenge. The capability to accurately predict the emergence of resistance, either to one or multiple drugs, may help to improve treatment options. Existing theoretical approaches often focus on exponential growth laws, which may not be realistic when scarce resources and competition limit growth. In this work, we study the emergence of single and double drug resistance in a model of combination therapy of two drugs. The model describes a sensitive strain, two types of single-resistant strains, and a double-resistant strain. We compare the probability that resistance emerges for three growth laws: exponential growth, logistic growth without competition between strains, and logistic growth with competition between strains. Using mathematical estimates and numerical simulations, we show that between-strain competition only affects the emergence of single resistance when resources are scarce. In contrast, the probability of double resistance is affected by between-strain competition over a wider space of resource availability. This indicates that competition between different resistant strains may be pertinent to identifying strategies for suppressing drug resistance, and that exponential models may overestimate the emergence of resistance to multiple drugs. A by-product of our work is an efficient strategy to evaluate probabilities of single and double resistance in models with multiple sequential mutations. This may be useful for a range of other problems in which the probability of resistance is of interest.

Published
2021

28. Mathematical modelling for antibiotic resistance control policy: do we know enough?

Author

Knight, Gwenan M., primary, Davies, Nicholas G., additional, Colijn, Caroline, additional, Coll, Francesc, additional, Donker, Tjibbe, additional, Gifford, Danna R., additional, Glover, Rebecca E., additional, Jit, Mark, additional, Klemm, Elizabeth, additional, Lehtinen, Sonja, additional, Lindsay, Jodi A., additional, Lipsitch, Marc, additional, Llewelyn, Martin J., additional, Mateus, Ana L. P., additional, Robotham, Julie V., additional, Sharland, Mike, additional, Stekel, Dov, additional, Yakob, Laith, additional, and Atkins, Katherine E., additional

Published
2019
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31. Spontaneous Mutation Rate Is a Plastic Trait Associated with Population Density across Domains of Life

Author

Rok Krašovec, Huw Richards, Gifford, Danna R., Charlie Hatcher, Katy Faulkner, Belavkin, Roman V., Alastair Channon, Elizabeth Aston, Mcbain, Andrew J., and Knight, Christopher G.

Subjects
QA75
Abstract

Rates of random, spontaneous mutation can vary plastically, dependent upon the environment. Such plasticity affects evolutionary trajectories and may be adaptive. We recently identified an inverse plastic association between mutation rate and population density at one locus in one species of bacterium. It is unknown how widespread this association is, whether it varies among organisms and what molecular mechanisms of mutagenesis or repair are required for this mutation rate plasticity. Here we address all three questions. We identify a strong negative association between mutation rate and population density across 70 years of published literature, comprising hundreds of mutation rates estimated using phenotypic markers of mutation (fluctuation tests) from all domains of life and viruses. We test this relationship experimentally, determining that there is indeed density-associated mutation-rate plasticity (DAMP) at multiple loci in both eukaryotes and bacteria, with up to 23-fold lower mutation rates at higher population densities. We find that the degree of plasticity varies, even among closely related organisms. Nonetheless, in each domain tested, DAMP requires proteins scavenging the mutagenic oxidized nucleotide 8-oxodGTP. This implies that phenotypic markers give a more precise view of mutation rate than previously believed: having accounted for other known factors affecting mutation rate, controlling for population density can reduce variation in mutation rate estimates by 93%. Widespread DAMP, which we manipulate genetically in disparate organisms, also provides a novel trait to use in the fight against the evolution of antimicrobial resistance. Such a prevalent environmental association and conserved mechanism suggest that mutation has varied plastically with population density since the early origins of life.

Published
2017
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39. Scaling fitness optima-Studying adaptive evolution with multiple genotypes of Aspergillus nidulans

Author

Gifford, Danna R

Subjects
Biology, General
Abstract

Adaptation involves the successive substitution of beneficial mutations by selection, a process known as an adaptive walk. Theoretical models of adaptation have made predictions regarding the properties of adaptive walks, but we know little empirically about how adaptation differs between different genotypes faced with the same environment, knowledge that is critical to a broad understanding of natural adaptation. Furthermore, as the body of theoretical knowledge continues to grow, it is becoming apparent that the conventional model systems used to study adaptation, chiefly single-celled organisms, are not well-suited for studying adaptation in spatially structured environments, and, barring yeasts, cannot be used to study the effects of sex on adaptation. This thesis tackles both questions using the fungus Aspergillus nidulans , first demonstrating that the selection coefficients of mutations, but not the total number, are affected by initial adaptedness to an environment and then developing a mathematical growth model that will allow for further development of theoretical models of adaptation in spatially structured environments.

Published
2013
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40. Here’s to the Losers: Evolvable Residents Accelerate the Evolution of High-Fitness Invaders

Author

Gifford, Danna R, Toll-Riera, Macarena, Kojadinovic, Mila, MacLean, R Craig; https://orcid.org/0000-0002-7941-813X, Gifford, Danna R, Toll-Riera, Macarena, Kojadinovic, Mila, and MacLean, R Craig; https://orcid.org/0000-0002-7941-813X

Abstract

Recent work has shown that evolvability plays a key role in determining the long-term population dynamics of asexual clones. However, simple considerations suggest that the evolvability of a focal lineage of bacteria should also be influenced by the evolvability of its competitors. First, evolvable competitors should accelerate evolution by impeding the fixation of the focal lineage through a clonal interference–like mechanism. Second, evolvable competitors should increase the strength of selection by rapidly degrading the environment, increasing selection for adaptive mutations. Here we tested these ideas by allowing a high-fitness clone of the bacterium Pseudomonas aeruginosa to invade populations of two low-fitness resident clones that differ in their evolvability. Both competition from mutations in the resident lineage and environmental degradation lead to faster adaptation in the invader through fixing single mutations with a greater fitness advantage. The results suggest that competition from mutations in both the successful invader and the unsuccessful resident shapes the adaptive trajectory of the invader through both direct competition and indirect environmental effects. Therefore, to predict evolutionary outcomes, it will be necessary to consider the evolvability of all members of the community and the effects of adaptation on the quality of the environment. This is particularly relevant to mixed microbial communities where lineages differ in their adaptive potential, a common feature of chronic infections.

Published
2015

41. Opposing effects of final population density and stress on Escherichia colimutation rate

Author

Krašovec, Rok, Richards, Huw, Gifford, Danna, Belavkin, Roman, Channon, Alastair, Aston, Elizabeth, McBain, Andrew, and Knight, Christopher

Abstract

Evolution depends on mutations. For an individual genotype, the rate at which mutations arise is known to increase with various stressors (stress-induced mutagenesis—SIM) and decrease at high final population density (density-associated mutation-rate plasticity—DAMP). We hypothesised that these two forms of mutation-rate plasticity would have opposing effects across a nutrient gradient. Here we test this hypothesis, culturing Escherichia coliin increasingly rich media. We distinguish an increase in mutation rate with added nutrients through SIM (dependent on error-prone polymerases Pol IV and Pol V) and an opposing effect of DAMP (dependent on MutT, which removes oxidised G nucleotides). The combination of DAMP and SIM results in a mutation rate minimum at intermediate nutrient levels (which can support 7 × 108cells ml−1). These findings demonstrate a strikingly close and nuanced relationship of ecological factors—stress and population density—with mutation, the fuel of all evolution.

Published
2018
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45. Investigations of microbial adaptation to singular, binary, and fully formulated quaternary ammonium compounds.

Author

Willmott, Thomas, Kelly, Paul P., Jadaan, Layali, Gifford, Danna R., Mercer, Steven D., Humphreys, Gavin J., Knight, Christopher G., Lu, Jian R., and McBain, Andrew J.

Subjects
*SINGLE nucleotide polymorphisms, *QUATERNARY ammonium compounds, *BIOCIDES, *DRUG resistance in bacteria, *MICROBIAL growth
Abstract

The study was conducted to inform risk assessments concerning microbial exposure to quaternary ammonium biocides (QUATs) by investigating their effects on 10 microbial strains of hygiene relevance. Biocides were divided into three categories: simple aqueous solutions, biocide mixtures, and formulated biocides. Organisms were grown in the presence of biocides for 10 generations and then subsequently for another 10 generations in biocide-free media. Control organisms were passaged 20 times in biocide-free media. Strains were then assessed for biocide and antibiotic susceptibility, changes in growth dynamics, and single nucleotide polymorphisms (SNPs). Biocide mixtures demonstrated greater antimicrobial potency than singular and formulated biocides. Susceptibility changes of under twofold were observed for all biocides tested. Susceptibility decreased significantly for organisms passaged with singular biocides (1.29-to 4.35-fold) and biocide mixtures (1.4- to 1.5-fold), but not for formulated biocides (1.3- to 1.84-fold) compared to controls. Antibiotic susceptibility both increased and decreased in passaged organisms, with heightened susceptibility occurring more frequently in the singular biocide group. Changes in susceptibility and growth dynamics were similar in the passaged and unexposed controls for fitness measures of adapted bacteria; there were no significant differences between biocide groups, but significant ly lower generation and doubling times in organisms exposed to singular biocides. Similar frequencies in SNPs occurred for the three biocide groups and unexposed controls. While some adaptations occurred, particularly with singular biocides, the impact on antibiotic resistance and genomic mutations was limited. These findings suggest that the use of formulated QUATs may pose a comparatively lower risk for antimicrobial resistance. IMPORTANCE Biocides are used globally to control microbial growth and effective assessment of the risks and benefits of their use is therefore a high priority. Much of the data used to assess risk has been based on sub-lethal exposure of bacteria to singular biocides in simple aqueous solutions. This work builds on limited prior realismbased studies to demonstrate enhanced potency in biocidal mixtures; the mitigation of resistance selection by formulations and inconsistent cross-resistance effects with both increases and decreases in susceptibility for a wide range of antibiotics. These data can be used to better inform risk assessments of biocide deployment. [ABSTRACT FROM AUTHOR]

Published
2024
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46. Stochastic dynamics of biological populations in changing environments

Author

Berríos, Ernesto, Galla, Tobias, and Gifford, Danna

Subjects
multi-drug resistance, biological populations, mating types evolution, stochastic dynamics, stochastic numerical simulations, individual-based models
Abstract

The focus of this thesis is the study of biological populations subject to external changing environments exploring a number of theoretical, numerical, and experimental approaches. We study different classes of environments, considering cases whose evolution over time is deterministic or stochastic. The first class of environments we consider vary deterministically. Here we focus on the study of microbial resistance in bacterial populations subject to therapies of one or two antibiotics. The environment specifies the drug concentration administered to the population, so it is determined by the type of dosing schedules. We investigate how subpopulations with higher mutation rates drive the emergence of multi-drug resistance. We approach this problem analysing experimental data (obtained by Dr. Danna Gifford), comparing their observations against stochastic simulations of a multi-type branching model we design. In separate work related to the previous one, we explore the delaying effect of competition on the emergence of single and double resistance through theoretical predictions of a similar stochastic model. We calculate the probability of having at least one resistant cell for dosing schedules with constant and time-dependent drug concentrations using a theoretical approach based on branching processes. The second class of environments we consider vary stochastically. The first system we study is a Moran-type model, describing a population subject to a switching environment that determines the type of reproduction, namely sexual or asexual. The population can exhibit several number of `mating types' (analog to male/female sexes, but not restricted to two) that depends on the rate of reproduction, as well as the mutation rate (i.e., inclusion of new types). We investigate the stationary distribution of the number of mating types for different switching regimes. We show that for slow switching regimes the distribution can become bimodal, while for fast switching the system behaves as if there was one single effective environment. Our approach exploits properties of branching processes and integer partitions in number theory. Lastly, we study and design an algorithm based on the so-called tau-leaping algorithm, focusing on systems with fast fluctuating environments. Our algorithm treats the input rates for the tau-leaping as (clipped) Gaussian random variables with first and second moments constructed from the environmental process. Several biological examples are explored, such as genetic circuits, birth-death processes, and genetic switches. We consider cases with discrete and continuous environmental spaces. The algorithm can produce results for macroscopic observables in fluctuating regimes beyond the adiabatic limit (i.e., infinitely fast switching) that are in good agreement with measurements from other simulation methods, but with a significantly reduced computing time.

Published
2021

47. Here’s to the losers: evolvable residents accelerate the evolution of high-fitness invaders

Author

Mila Kojadinovic, Macarena Toll-Riera, R. Craig MacLean, Danna R. Gifford, University of Zurich, Gifford, Danna R, University of Cambridge [UK] (CAM), Institute of Evolutionary Biology and Environmental Studies, Universität Zürich [Zürich] = University of Zurich (UZH), Aix Marseille Université (AMU), Bioénergétique et Ingénierie des Protéines (BIP ), and Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
0106 biological sciences, Evolution, media_common.quotation_subject, [SDV]Life Sciences [q-bio], Population, Population Dynamics, Genetic Fitness, Genetic mutation, Biology, medicine.disease_cause, Biological adaptation, 010603 evolutionary biology, 01 natural sciences, Competition (biology), 03 medical and health sciences, 10127 Institute of Evolutionary Biology and Environmental Studies, medicine, Sequencing, Genomes, education, Ecology, Evolution, Behavior and Systematics, 030304 developmental biology, media_common, Genetics, 0303 health sciences, Mutation, Experimental evolution, education.field_of_study, Models, Genetic, T tests, Adaptation, Physiological, Biological Evolution, Environmental degradation, Evolvability, Fixation (population genetics), Genetics, Population, 1105 Ecology, Evolution, Behavior and Systematics, Genes, Pseudomonas aeruginosa, Ecological competition, Epistasis, 570 Life sciences, biology, 590 Animals (Zoology), Natural resources
Abstract

International audience; AbstractRecent work has shown that evolvability plays a key role in determining the long-term population dynamics of asexual clones. However, simple considerations suggest that the evolvability of a focal lineage of bacteria should also be influenced by the evolvability of its competitors. First, evolvable competitors should accelerate evolution by impeding the fixation of the focal lineage through a clonal interference–like mechanism. Second, evolvable competitors should increase the strength of selection by rapidly degrading the environment, increasing selection for adaptive mutations. Here we tested these ideas by allowing a high-fitness clone of the bacterium Pseudomonas aeruginosa to invade populations of two low-fitness resident clones that differ in their evolvability. Both competition from mutations in the resident lineage and environmental degradation lead to faster adaptation in the invader through fixing single mutations with a greater fitness advantage. The results suggest that competition from mutations in both the successful invader and the unsuccessful resident shapes the adaptive trajectory of the invader through both direct competition and indirect environmental effects. Therefore, to predict evolutionary outcomes, it will be necessary to consider the evolvability of all members of the community and the effects of adaptation on the quality of the environment. This is particularly relevant to mixed microbial communities where lineages differ in their adaptive potential, a common feature of chronic infections.

Published
2015
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48. Adaptation at the Extremes of Life: Experimental Evolution with the Extremophile Archaeon Sulfolobus acidocaldarius.

Author

Al-Baqsami Z, Lowry Palmer R, Darwent G, McBain AJ, Knight CG, and Gifford DR

Subjects
Extremophiles physiology, Adaptation, Physiological physiology, Batch Cell Culture Techniques methods, Batch Cell Culture Techniques instrumentation, Sulfolobus acidocaldarius
Abstract

The archaeon Sulfolobus acidocaldarius has emerged as a promising thermophilic model system. Investigating how thermophiles adapt to changing temperatures is a key requirement, not only for understanding fundamental evolutionary processes but also for developing S. acidocaldarius as a chassis for bioengineering. One major obstacle to conducting experimental evolution with thermophiles is the expense of equipment maintenance and energy usage of traditional incubators for high-temperature growth. To address this challenge, a comprehensive experimental protocol for conducting experimental evolution in S. acidocaldarius is presented, utilizing low-cost and energy-efficient bench-top thermomixers. The protocol involves a batch culture technique with relatively small volumes (1.5 mL), enabling tracking of adaptation in multiple independent lineages. This method is easily scalable through the use of additional thermomixers. Such an approach increases the accessibility of S. acidocaldarius as a model system by reducing both initial investment and ongoing costs associated with experimental investigations. Moreover, the technique is transferable to other microbial systems for exploring adaptation to diverse environmental conditions.

Published
2024
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