scholarly journals The effect of spatial structure on adaptation in Escherichia coli

2007 ◽  
Vol 4 (1) ◽  
pp. 57-59 ◽  
Author(s):  
Lilia Perfeito ◽  
M. Inês Pereira ◽  
Paulo R.A Campos ◽  
Isabel Gordo
Keyword(s):  
Escherichia Coli ◽  
Spatial Structure ◽  
Experimental Evolution ◽  
Petri Dish ◽  
Mutation Rates ◽  
Wild Type ◽  
Clonal Interference ◽  
Genetic Studies ◽  
Significant Difference ◽  
The Cost

Populations of organisms are generally organized in a given spatial structure. However, the vast majority of population genetic studies are based on populations in which every individual competes globally. Here we use experimental evolution in Escherichia coli to directly test a recently made prediction that spatial structure slows down adaptation and that this cost increases with the mutation rate. This was studied by comparing populations of different mutation rates adapting to a liquid (unstructured) medium with populations that evolved in a Petri dish on solid (structured) medium. We find that mutators adapt faster to both environments and that adaptation is slower if there is spatial structure. We observed no significant difference in the cost of structure between mutator and wild-type populations, which suggests that clonal interference is intense in both genetic backgrounds.

Fitness Evolution and the Rise of Mutator Alleles in Experimental Escherichia coli Populations

Genetics ◽  
2002 ◽  
Vol 162 (2) ◽  
pp. 557-566 ◽  
Author(s):  
Aaron C Shaver ◽  
Peter G Dombrowski ◽  
Joseph Y Sweeney ◽  
Tania Treis ◽  
Renata M Zappala ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Genetic Drift ◽  
Mutation Rates ◽  
Significant Gain ◽  
Wild Type ◽  
Clonal Interference ◽  
Beneficial Mutations ◽  
Mutator Allele ◽  
Experimental Populations ◽  
Rate Of Substitution

Abstract We studied the evolution of high mutation rates and the evolution of fitness in three experimental populations of Escherichia coli adapting to a glucose-limited environment. We identified the mutations responsible for the high mutation rates and show that their rate of substitution in all three populations was too rapid to be accounted for simply by genetic drift. In two of the populations, large gains in fitness relative to the ancestor occurred as the mutator alleles rose to fixation, strongly supporting the conclusion that mutator alleles fixed by hitchhiking with beneficial mutations at other loci. In one population, no significant gain in fitness relative to the ancestor occurred in the population as a whole while the mutator allele rose to fixation, but a substantial and significant gain in fitness occurred in the mutator subpopulation as the mutator neared fixation. The spread of the mutator allele from rarity to fixation took >1000 generations in each population. We show that simultaneous adaptive gains in both the mutator and wild-type subpopulations (clonal interference) retarded the mutator fixation in at least one of the populations. We found little evidence that the evolution of high mutation rates accelerated adaptation in these populations.

scholarly journals Local adaptation mediated niche expansion in correlation with genetic richness

2021 ◽  
Author(s):  
Masaomi Kurokawa ◽  
Issei Nishimura ◽  
Bei-Wen YING
Keyword(s):  
Escherichia Coli ◽  
Local Adaptation ◽  
High Throughput ◽  
Experimental Evolution ◽  
Environmental Gradient ◽  
Growth Curves ◽  
Quantitative Relationship ◽  
Central Issue ◽  
Wild Type ◽  
Niche Expansion

As a central issue in evolution and ecology, the quantitative relationship among the genome, adaptation and the niche was investigated. Local adaptation of five Escherichia coli strains carrying either the wild-type genome or reduced genomes was achieved by experimental evolution. A high-throughput fitness assay of the ancestor and evolved populations across an environmental gradient of eight niches resulted in a total of 80 fitness curves generated from 2,220 growth curves. Further analyses showed that the increases in both local adaptiveness and niche broadness were negatively correlated with genetic richness. Local adaptation caused common niche expansion, whereas niche expansion for generality or speciality was decided by genetic richness. The order of the mutations accumulated stepwise was correlated with the magnitude of the fitness increase attributed to mutation accumulation. Pre-adaptation probably participated in coordination among genetic richness, local adaptation and niche expansion.

scholarly journals Resistance/fitness trade-off is a barrier to the evolution of MarR inactivation mutants in Escherichia coli

2020 ◽  
Vol 76 (1) ◽  
pp. 77-83 ◽  
Author(s):  
Lisa Praski Alzrigat ◽  
Douglas L Huseby ◽  
Gerrit Brandis ◽  
Diarmaid Hughes
Keyword(s):  
Escherichia Coli ◽  
Experimental Evolution ◽  
Efflux Pump ◽  
Drug Susceptibility ◽  
Fitness Cost ◽  
Competitive Growth ◽  
Contributing Factors ◽  
Trade Off ◽  
Compensatory Evolution ◽  
The Cost

Abstract Background Mutations that inactivate MarR reduce susceptibility to ciprofloxacin and competitive growth fitness in Escherichia coli. Both phenotypes are caused by overexpression of the MarA regulon, which includes the AcrAB-TolC drug efflux pump. Objectives We asked whether compensatory evolution could reduce the fitness cost of MarR-inactivating mutations without affecting resistance to ciprofloxacin. Methods The cost of overexpressing the AcrAB-TolC efflux pump was measured independently of MarA overexpression. Experimental evolution of MarR-inactive strains was used to select mutants with increased fitness. The acquired mutations were identified and their effects on drug susceptibility were measured. Results Overexpression of the AcrAB-TolC efflux pump was found not to contribute to the fitness cost of MarA regulon overexpression. Fitness-compensatory mutations were selected in marA and lon. The mutations reduced the level of MarA protein thus reducing expression of the MarA regulon. They restored growth fitness but also reduced resistance to ciprofloxacin. Conclusions The fitness cost caused by overexpression of the MarA regulon has multiple contributing factors. Experimental evolution did not identify any single pump-independent cost factor. Instead, efficient fitness compensation occurred only by mechanisms that reduce MarA concentration, which simultaneously reduce the drug resistance phenotype. This resistance/fitness trade-off is a barrier to the successful spread of MarR inactivation mutations in clinical isolates where growth fitness is essential.

scholarly journals Reversal of Flagellar Rotation Is Important in Initial Attachment of Escherichia coli to Glass in a Dynamic System with High- and Low-Ionic-Strength Buffers

2002 ◽  
Vol 68 (3) ◽  
pp. 1280-1289 ◽  
Author(s):  
Jennifer W. McClaine ◽  
Roseanne M. Ford
Keyword(s):  
Escherichia Coli ◽  
Ionic Strength ◽  
Cell Attachment ◽  
Fluid Velocity ◽  
Soft Particle ◽  
Wild Type ◽  
Buffer Solutions ◽  
Fluid Velocities ◽  
Significant Difference ◽  
Flagellar Rotation

ABSTRACT The attachment rates of wild-type, smooth-swimming, tumbly, and paralyzed Escherichia coli to glass was measured at fluid velocities of 0.0044 and 0.044 cms−1 (corresponding to shear rates of 0.34 and 3.4 s−1, respectively), in 0.02 and 0.2 M buffer solutions. At the highest ionic strength, we did not observe a significant difference in the attachment rate of wild-type and paralyzed cells at either fluid velocity. However, when the ionic strength was reduced, paralyzed bacteria attached at rates 4 and 10 times lower than that of the wild type under fluid velocities of 0.0044 and 0.044 cms−1, respectively. This suggested that the rotation of the flagella assisted in attachment. We then compared the attachment rates of smooth-swimming (counterclockwise rotation only) and tumbly (clockwise rotation only) cells to the wild type to determine whether the direction of rotation was important to cell attachment. At 0.0044 cms−1, the smooth-swimming cells attached at rates similar to that of the wild type in both buffer solutions but significantly less at the higher fluid velocity. Tumbly cells attached at much lower rates under all conditions. Thus, the combination of clockwise and counterclockwise flagellar rotation and their coupling appeared to be important in cell attachment. We considered a number of hypotheses to interpret these observations, including a residence time analysis and a comparison of traditional Derjaguin-Landau-Verwey-Overbeek (DLVO) theory to soft-particle theory.

scholarly journals Sociality in Escherichia coli: Enterochelin Is a Private Good at Low Cell Density and Can Be Shared at High Cell Density

2015 ◽  
Vol 197 (13) ◽  
pp. 2122-2128 ◽  
Author(s):  
Rebecca L. Scholz ◽  
E. Peter Greenberg
Keyword(s):  
Escherichia Coli ◽  
Cell Density ◽  
Iron Acquisition ◽  
Partial Privatization ◽  
High Cell ◽  
Wild Type ◽  
Content Type ◽  
Cell Densities ◽  
The Cost ◽  
Low Cell Density

ABSTRACTMany bacteria produce secreted iron chelators called siderophores, which can be shared among cells with specific siderophore uptake systems regardless of whether the cell produces siderophores. Sharing secreted products allows freeloading, where individuals use resources without bearing the cost of production. Here we show that theEscherichia colisiderophore enterochelin is not evenly shared between producers and nonproducers. Wild-typeEscherichia coligrows well in low-iron minimal medium, and an isogenic enterochelin synthesis mutant (ΔentF) grows very poorly. The enterochelin mutant grows well in low-iron medium supplemented with enterochelin. At high cell densities the ΔentFmutant can compete equally with the wild type in low-iron medium. At low cell densities the ΔentFmutant cannot compete. Furthermore, the growth rate of the wild type is unaffected by cell density. The wild type grows well in low-iron medium even at very low starting densities. Our experiments support a model where at least some enterochelin remains associated with the cells that produce it, and the cell-associated enterochelin enables iron acquisition even at very low cell density. Enterochelin that is not retained by producing cells at low density is lost to dilution. At high cell densities, cell-free enterochelin can accumulate and be shared by all cells in the group. Partial privatization is a solution to the problem of iron acquisition in low-iron, low-cell-density habitats. Cell-free enterochelin allows for iron scavenging at a distance at higher population densities. Our findings shed light on the conditions under which freeloaders might benefit from enterochelin uptake systems.IMPORTANCESociality in microbes has become a topic of great interest. One facet of sociality is the sharing of secreted products, such as the iron-scavenging siderophores. We present evidence that theEscherichia colisiderophore enterochelin is relatively inexpensive to produce and is partially privatized such that it can be efficiently shared only at high producer cell densities. At low cell densities, cell-free enterochelin is scarce and only enterochelin producers are able to grow in low-iron medium. Because freely shared products can be exploited by freeloaders, this partial privatization may help explain how enterochelin production is stabilized inE. coliand may provide insight into when enterochelin is available for freeloaders.

scholarly journals Role of CheB and CheR in the Complex Chemotactic and Aerotactic Pathway of Azospirillum brasilense

2006 ◽  
Vol 188 (13) ◽  
pp. 4759-4768 ◽  
Author(s):  
Bonnie B. Stephens ◽  
Star N. Loar ◽  
Gladys Alexandre
Keyword(s):  
Escherichia Coli ◽  
Steady State ◽  
Azospirillum Brasilense ◽  
Model Organism ◽  
Spatial Gradient ◽  
Wild Type ◽  
Temporal Gradient ◽  
E Coli ◽  
Significant Difference

ABSTRACT It has previously been reported that the alpha-proteobacterium Azospirillum brasilense undergoes methylation-independent chemotaxis; however, a recent study revealed cheB and cheR genes in this organism. We have constructed cheB, cheR, and cheBR mutants of A. brasilense and determined that the CheB and CheR proteins under study significantly influence chemotaxis and aerotaxis but are not essential for these behaviors to occur. First, we found that although cells lacking CheB, CheR, or both were no longer capable of responding to the addition of most chemoattractants in a temporal gradient assay, they did show a chemotactic response (albeit reduced) in a spatial gradient assay. Second, in comparison to the wild type, cheB and cheR mutants under steady-state conditions exhibited an altered swimming bias, whereas the cheBR mutant and the che operon mutant did not. Third, cheB and cheR mutants were null for aerotaxis, whereas the cheBR mutant showed reduced aerotaxis. In contrast to the swimming bias for the model organism Escherichia coli, the swimming bias in A. brasilense cells was dependent on the carbon source present and cells released methanol upon addition of some attractants and upon removal of other attractants. In comparison to the wild type, the cheB, cheR, and cheBR mutants showed various altered patterns of methanol release upon exposure to attractants. This study reveals a significant difference between the chemotaxis adaptation system of A. brasilense and that of the model organism E. coli and suggests that multiple chemotaxis systems are present and contribute to chemotaxis and aerotaxis in A. brasilense.

Drug cost and outcome in metastatic colorectal cancer with emphasis on monoclonal antibodies.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 567-567
Author(s):  
Helmy M. Guirgis
Keyword(s):  
Colorectal Cancer ◽  
Monoclonal Antibodies ◽  
Metastatic Colorectal Cancer ◽  
Drug Cost ◽  
Outcome Evaluation ◽  
Wild Type ◽  
First Line ◽  
Significant Difference ◽  
Number Of Cycles ◽  
The Cost

567 Background: Patients with wild type KRAS metastatic colorectal cancer (mCRC), treated with first-line cetuximab (Cet) or bevacizumab (Bev) and chemotherapy demonstrated similar overall survival (OS). In the Western world, costs of anticancer drugs ranged from $59,000 to $100,000 per life-year gain (LYG). Hazard ratios (HR) have rarely been integrated in cost/outcome evaluation. Objective: Weigh drug cost against survival and hazard ratio (HR) in mCRC with emphasis on monoclonal antibodies (MABs). Methods: Estimated costs in United States dollars (US$) were calculated for 70 kg or 1.7/m2 patients. Costs were divided by the reported median OS gain over control in days (OSg) and by probability of survival (PoS) calculated as (1.0 – HR). Relative values (RV) were computed as 100,000/cost/outcome. Results: There was no significant difference in cost/outcome of Pan and Cet in first-line wild KRAS mCRC. At 12 week (w), the cost/LYG of panitumumab (Pan), Cet, and Bev were $64,947, $82,224, and $36,919 with RVs of 1.54, 1.22 and 2.71 respectively. Using HRs, the corresponding PoS were $140,082, $137,040, and $42,524 with RVs of 0.71, 0.73, and 2.35. Wild RAS testing improved the cost/outcome of Pan by 25%. Increasing number of cycles increased the cost/outcome and decreased the RVs of all MOAs. Conclusions: In first-line wild KRAS mCRC at 12 w, the cost/outcome of Bev was approximately 30% to 57% that of Pan and Cet. Cost/outcome of Pan significantly improved in RAS wild type. The cost/outcome of MABs was determined by the number of cycles.

scholarly journals GlpD and PlsB Participate in Persister Cell Formation in Escherichia coli

2006 ◽  
Vol 188 (14) ◽  
pp. 5136-5144 ◽  
Author(s):  
Amy L. Spoering ◽  
Marin Vulić ◽  
Kim Lewis
Keyword(s):  
Escherichia Coli ◽  
Cell Formation ◽  
Wild Type ◽  
Expression Library ◽  
Genetic Studies ◽  
Bacterial Populations ◽  
E Coli ◽  
Overexpression Strain ◽  
Multidrug Tolerance ◽  
Glycerol 3 Phosphate Dehydrogenase

ABSTRACT Bacterial populations produce dormant persister cells that are resistant to killing by all antibiotics currently in use, a phenomenon known as multidrug tolerance (MDT). Persisters are phenotypic variants of the wild type and are largely responsible for MDT of biofilms and stationary populations. We recently showed that a hipBA toxin/antitoxin locus is part of the MDT mechanism in Escherichia coli. In an effort to find additional MDT genes, an E. coli expression library was selected for increased survival to ampicillin. A clone with increased persister production was isolated and was found to overexpress the gene for the conserved aerobic sn-glycerol-3-phosphate dehydrogenase GlpD. The GlpD overexpression strain showed increased tolerance to ampicillin and ofloxacin, while a strain with glpD deleted had a decreased level of persisters in the stationary state. This suggests that GlpD is a component of the MDT mechanism. Further genetic studies of mutants affected in pathways involved in sn-glycerol-3-phosphate metabolism have led to the identification of two additional multidrug tolerance loci, glpABC, the anaerobic sn-glycerol-3-phosphate dehydrogenase, and plsB, an sn-glycerol-3-phosphate acyltransferase.

scholarly journals Loss of Resistance to Ingestion and Phagocytic Killing by O− and K− Mutants of a Uropathogenic Escherichia coli O75:K5 Strain

1999 ◽  
Vol 67 (8) ◽  
pp. 3757-3762 ◽  
Author(s):  
Stacy M. Burns ◽  
Sheila I. Hull
Keyword(s):  
Escherichia Coli ◽  
Polymorphonuclear Leukocytes ◽  
Wild Type Strain ◽  
Uropathogenic Escherichia Coli ◽  
Wild Type ◽  
O Antigen ◽  
Loss Of Resistance ◽  
Significant Difference ◽  
The Difference ◽  
Phagocytic Killing

ABSTRACT To determine the importance of the O75 O antigen and the K5 capsular antigen in resistance to phagocytosis and phagocytic killing, we used previously described O75− and K5−mutants from an O75+ K5+ wild-type uropathogenic Escherichia coli strain in phagocytosis assays with polymorphonuclear leukocytes (PMNs) and monocytes. At a 10-to-1 ratio of bacteria to phagocytes and in the presence of 10% serum, the parental strain GR-12 was resistant to both PMNs and monocytes over a 2-h incubation period. The O75− and K5− mutants were similar in sensitivity to killing by both PMNs and monocytes, decreasing in viability by 80% in the first hour. Yet, a significant difference in killing between the O75−and K5− mutants was observed in the first 15 min of incubation. The K5− mutant decreased in numbers by almost 60%, while the O75− mutant increased in numbers similarly to GR-12 in the first 15 min. The difference in killing was found not to be due to the rate of opsonization. To further determine the mechanism of resistance, a fluorescence assay was used to differentiate attached and internalized bacteria. The K5 capsule hindered the association of both the wild-type strain and the O75−mutant in the initial incubation time with PMNs. In conclusion, both the K5 capsule and O75 O antigen play crucial roles in resistance to phagocytosis over time.

Sign in / Sign up

Export Citation Format

Share Document