scholarly journals The Effects of Evolution and Spatial Structure on Diversity in Biological Reserves

2016 ◽  
Author(s):  
Emily Louise Dolson ◽  
Michael J Wiser ◽  
Charles A Ofria

Conservation ecologists have long argued over the best way of placing reserves across an environment to maximize population diversity. Many have studied the effect of protecting many small regions of an ecosystem vs. a single large region, with varied results. However, this research tends to ignore evolutionary dynamics under the rationale that the spatiotemporal scale required is prohibitive. We used the Avida digital evolution research platform to overcome this barrier and study the response of phenotypic diversity to eight different reserve placement configurations. The capacity for mutation,and therefore evolution, substantially altered the dynamics of diversity in the population. When mutations were allowed, reserve configurations involving a greater number of consequently smaller reserves were substantially more effective at maintaining existing diversity and generating new diversity. However, when mutations were disallowed, reserve configuration had little effect on diversity generation and maintenance. While further research is necessary before translating these results into policy decisions, this study demonstrates the importance of considering evolution when making such decisions and suggests that a larger number of smaller reserves may have evolutionary benefits.

2017 ◽  
Vol 91 (22) ◽  
Author(s):  
Christopher B. Brooke

ABSTRACT Influenza A virus (IAV) continues to pose an enormous and unpredictable global public health threat, largely due to the continual evolution of escape from preexisting immunity and the potential for zoonotic emergence. Understanding how the unique genetic makeup and structure of IAV populations influences their transmission and evolution is essential for developing more-effective vaccines, therapeutics, and surveillance capabilities. Owing to their mutation-prone replicase and unique genome organization, IAV populations exhibit enormous amounts of diversity both in terms of sequence and functional gene content. Here, I review what is currently known about the genetic and genomic diversity present within IAV populations and how this diversity may shape the replicative and evolutionary dynamics of these viruses.


PLoS Biology ◽  
2020 ◽  
Vol 18 (12) ◽  
pp. e3000987
Author(s):  
Clare L. Kinnear ◽  
Elsa Hansen ◽  
Valerie J. Morley ◽  
Kevin C. Tracy ◽  
Meghan Forstchen ◽  
...  

The antimicrobial resistance crisis has persisted despite broad attempts at intervention. It has been proposed that an important driver of resistance is selection imposed on bacterial populations that are not the intended target of antimicrobial therapy. But to date, there has been limited quantitative measure of the mean and variance of resistance following antibiotic exposure. Here we focus on the important nosocomial pathogen Enterococcus faecium in a hospital system where resistance to daptomycin is evolving despite standard interventions. We hypothesized that the intravenous use of daptomycin generates off-target selection for resistance in transmissible gastrointestinal (carriage) populations of E. faecium. We performed a cohort study in which the daptomycin resistance of E. faecium isolated from rectal swabs from daptomycin-exposed patients was compared to a control group of patients exposed to linezolid, a drug with similar indications. In the daptomycin-exposed group, daptomycin resistance of E. faecium from the off-target population was on average 50% higher than resistance in the control group (n = 428 clones from 22 patients). There was also greater phenotypic diversity in daptomycin resistance within daptomycin-exposed patients. In patients where multiple samples over time were available, a wide variability in temporal dynamics were observed, from long-term maintenance of resistance to rapid return to sensitivity after daptomycin treatment stopped. Sequencing of isolates from a subset of patients supports the argument that selection occurs within patients. Our results demonstrate that off-target gastrointestinal populations rapidly respond to intravenous antibiotic exposure. Focusing on the off-target evolutionary dynamics may offer novel avenues to slow the spread of antibiotic resistance.


2019 ◽  
Author(s):  
Michelle C. Stitzer ◽  
Sarah N. Anderson ◽  
Nathan M. Springer ◽  
Jeffrey Ross-Ibarra

Transposable elements (TEs) constitute the majority of flowering plant DNA, reflecting their tremendous success in subverting, avoiding, and surviving the defenses of their host genomes to ensure their selfish replication. More than 85% of the sequence of the maize genome can be ascribed to past transposition, providing a major contribution to the structure of the genome. Evidence from individual loci has informed our understanding of how transposition has shaped the genome, and a number of individual TE insertions have been causally linked to dramatic phenotypic changes. But genome-wide analyses in maize and other taxa have frequently represented TEs as a relatively homogeneous class of fragmentary relics of past transposition, obscuring their evolutionary history and interaction with their host genome. Using an updated annotation of structurally intact TEs in the maize reference genome, we investigate the family-level ecological and evolutionary dynamics of TEs in maize. Integrating a variety of data, from descriptors of individual TEs like coding capacity, expression, and methylation, as well as similar features of the sequence they inserted into, we model the relationship between these attributes of the genomic environment and the survival of TE copies and families. Our analyses reveal a diversity of ecological strategies of TE families, each representing the evolution of a distinct ecological niche allowing survival of the TE family. In contrast to the wholesale relegation of all TEs to a single category of junk DNA, these differences generate a rich ecology of the genome, suggesting families of TEs that coexist in time and space compete and cooperate with each other. We conclude that while the impact of transposition is highly family- and context-dependent, a family-level understanding of the ecology of TEs in the genome can refine our ability to predict the role of TEs in generating genetic and phenotypic diversity.‘Lumping our beautiful collection of transposons into a single category is a crime’-Michael R. Freeling, Mar. 10, 2017


2005 ◽  
Vol 15 (11) ◽  
pp. 1619-1638 ◽  
Author(s):  
ROBERT A. GATENBY ◽  
THOMAS L. VINCENT ◽  
ROBERT J. GILLIES

We have previously demonstrated intra- and extra-cellular factors that govern somatic evolution of the malignant phenotype can be modeled through evolutionary game theory, a mathematical approach that analyzes phenotypic adaptation to in-vivo environmental selection forces. Here we examine the global evolutionary dynamics that control evolutionary dynamics explicitly addressing conflicting data and hypothesis regarding the relative importance of the mutator phenotype and microenvironment controls. We find evolution of invasive cancer follows a biphasic pattern. The first phase occurs within normal tissue, which possesses a remarkable adaptive landscape that permits non-competitive coexistence of multiple cellular populations but renders it vulnerable to invasion. When random genetic mutations produce a fitter phenotype, self-limited clonal expansion is observed — equivalent to a polyp or nevus. This step corresponds to tumor initiation in classical skin carcinogenesis experiments because the mutant population deforms the adaptive landscape resulting in the emergence of unoccupied fitness peaks — a premalignant configuration because, over time, extant cellular populations will tend to evolve toward available fitness maxima forming an invasive cancer. We demonstrate that this phase is governed by intracellular processes, such as the mutation rate, that promote phenotypic diversity and environmental factors that control cellular selection and population growth. These results provide an integrative model of carcinogenesis that incorporates cell-centric approaches such as the mutator phenotype hypothesis with the critical role of the environmental demonstrated by Bissell and others. The biphasic dynamics of carcinogenesis give a quantitative framework of understanding for the empirically observed initiation and promotion/progression stages in skin carcinogenesis experimental models.


2017 ◽  
Author(s):  
WR Shoemaker ◽  
JT Lennon

ABSTRACTDormancy is a bet-hedging strategy that allows organisms to persist through conditions that are sub-optimal for growth and reproduction by entering a reversible state of reduced metabolic activity. Dormancy allows a population to maintain a reservoir of genetic and phenotypic diversity (i.e., a seed bank) that can contribute to the long-term survival of a population. This strategy can be potentially adaptive and has long been of interest to ecologists and evolutionary biologists. However, comparatively little is known about how dormancy influences the fundamental evolutionary forces of genetic drift, mutation, selection, recombination, and gene flow. Here, we investigate how seed banks affect the processes underpinning evolution by reviewing existing theory, implementing novel simulations, and determining how and when dormancy can influence evolution as a population genetic process. We extend our analysis to examine how seed banks can alter macroevolutionary processes, including rates of speciation and extinction. Through the lens of population genetic theory, we can understand the extent that seed banks influence microbial evolutionary dynamics.


2017 ◽  
Author(s):  
Bryan T. Weinstein ◽  
Maxim O. Lavrentovich ◽  
Wolfram Möbius ◽  
Andrew W. Murray ◽  
David R. Nelson

AbstractWe experimentally and numerically investigate the evolutionary dynamics of four competing strains of E. coli with differing expansion velocities in radially expanding colonies. We compare experimental measurements of the average fraction, correlation functions between strains, and the relative rates of genetic domain wall annihilations and coalescences to simulations modeling the population as a one-dimensional ring of annihilating and coalescing random walkers with deterministic biases due to selection. The simulations reveal that the evolutionary dynamics can be collapsed onto master curves governed by three essential parameters: (1) an expansion length beyond which selection dominates over genetic drift; (2) a characteristic angular correlation describing the size of genetic domains; and (3) a dimensionless constant quantifying the interplay between a colony’s curvature at the frontier and its selection length scale. We measure these parameters with a new technique that precisely measures small selective differences between spatially competing strains and show that our simulations accurately predict the dynamics with no additional fitting. Our results suggest that that the random walk model can act as a useful predictive tool when describing the evolutionary dynamics of range expansions composed of an arbitrary number of competing alleles with different fitnesses.Author summaryPopulation expansions occur naturally during the spread of invasive species and have played a role in our evolutionary history when many of our ancestors expanded out of Africa. We use a colony of bacteria expanding into unoccupied, nutrient-rich territory on an agar plate as a model system to explore how an expanding population’s spatial structure impacts its evolutionary dynamics. Spatial structure is present in expanding microbial colonies because daughter cells migrate only a small distance away from their mothers each generation. Generally, the constituents of expansions occurring in nature and in the lab have different genetic compositions (genotypes, or alleles if a single gene differs), each instilling different fitnesses, which compete to proliferate at the frontier. Here, we show that a random-walk model can accurately predict the dynamics of four expanding strains of E. coli with different fitnesses; each strain represents a competing allele. Our results can be extended to describe any number of competing genotypes with different fitnesses in a naturally occurring expansions. Our model can also be used to precisely measure small selective differences between spatially competing genotypes in controlled laboratory settings.


2016 ◽  
Author(s):  
Jia-Xing Yue ◽  
Jing Li ◽  
Louise Aigrain ◽  
Johan Hallin ◽  
Karl Persson ◽  
...  

AbstractStructural rearrangements have long been recognized as an important source of genetic variation with implications in phenotypic diversity and disease, yet their evolutionary dynamics are difficult to characterize with short-read sequencing. Here, we report long-read sequencing for 12 strains representing major subpopulations of the partially domesticated yeastSaccharomyces cerevisiaeand its wild relativeSaccharomyces paradoxus. Complete genome assemblies and annotations generate population-level reference genomes and allow for the first explicit definition of chromosome partitioning into cores, subtelomeres and chromosome-ends. High-resolution view of structural dynamics uncovers that, in chromosomal cores,S. paradoxusexhibits higher accumulation rate of balanced structural rearrangements (inversions, translocations and transpositions) whereasS. cerevisiaeaccumulates unbalanced rearrangements (large insertions, deletions and duplications) more rapidly. In subtelomeres, recurrent interchromosomal reshuffling was found in both species, with higher rate inS. cerevisiae. Such striking contrasts between wild and domesticated yeasts reveal the influence of human activities on structural genome evolution.


2021 ◽  
Author(s):  
Yang Ping Kuo ◽  
César Nombela Arrieta ◽  
Oana Carja

AbstractUnderstanding how the spatial arrangement of a population shapes its evolutionary dynamics has been of long-standing interest in population genetics. Most previous studies assume a small number of demes connected by migration corridors, symmetrical structures that most often act as well-mixed populations. Other studies use networks to model the more complex topologies of natural populations and to study the structures that suppress or amplify selection. However, they usually assume very small, regular networks, with strong constraints on the strength of selection considered. Here we build network generation algorithms, evolutionary simulations and derive general analytic approximations for probabilities of fixation in populations with complex spatial structure. By tuning network parameters and properties independent of each other, we systematically span across network families and show that both a network’s degree distribution, as well as its node mixing pattern shape the evolutionary dynamics of new mutations. We analytically write the relevant selective parameter, predictive of evolutionary dynamics, as a combination of network statistics. As one application, we use recent imaging datasets and build the cellular spatial networks of the stem cell niches of the bone marrow. Across a wide variety of parameters and regardless of the birth-death process used, we find these networks to be strong suppressors of selection, delaying mutation accumulation in this tissue. We also find that decreases in stem cell population size decrease the suppression strength of the tissue spatial structure, hinting at a potential diminishing spatial suppression in the bone marrow tissue as individuals age.


mBio ◽  
2019 ◽  
Vol 10 (4) ◽  
Author(s):  
Erin S. Gloag ◽  
Christopher W. Marshall ◽  
Daniel Snyder ◽  
Gina R. Lewin ◽  
Jacob S. Harris ◽  
...  

ABSTRACT Opportunistic pathogens establishing new infections experience strong selection to adapt, often favoring mutants that persist. Capturing this initial dynamic is critical for identifying the first adaptations that drive pathogenesis. Here we used a porcine full-thickness burn wound model of chronic infection to study the evolutionary dynamics of diverse Pseudomonas aeruginosa infections. Wounds were infected with a mixed community of six P. aeruginosa strains, including the model PA14 strain (PA14-1), and biopsies taken at 3, 14, and 28 days postinfection. Hyperbiofilm-forming rugose small-colony variants (RSCVs) were the earliest and predominant phenotypic variant. These variants were detected on day 3 and persisted, with the majority evolved from PA14-1. Whole-genome sequencing of PA14-1 RSCV isolates revealed driver mutations exclusively in the wsp pathway, conferring hyperbiofilm phenotypes. Several of the wsp mutant RSCVs also acquired CRISPR-Cas adaptive immunity to prophages isolated from the P. aeruginosa wound isolate (B23-2) that was also present in the inoculum. These observations emphasize the importance of interstrain dynamics and the role of lysogenic phages in the survival of an invading pathogen. Rather than being a side effect of chronicity, the rapid rise of RSCVs in wounds is evidence of positive selection on the Wsp chemosensory system to produce mutants with elevated biofilm formation capacity. We predict that RSCVs provide a level of phenotypic diversity to the infecting bacterial community and are common, early adaptations during infections. This would likely have significant consequences for clinical outcomes. IMPORTANCE Bacteria adapt to infections by evolving variants that are more fit and persistent. These recalcitrant variants are typically observed in chronic infections. However, it is unclear when and why these variants evolve. To address these questions, we used a porcine chronic wound model to study the evolutionary dynamics of Pseudomonas aeruginosa in a mixed-strain infection. We isolated hyperbiofilm variants that persisted early in the infection. Interstrain interactions were also observed, where adapted variants acquired CRISPR-mediated immunity to phages. We show that when initiating infection, P. aeruginosa experiences strong positive selection for hyperbiofilm phenotypes produced by mutants of a single chemosensory system, the Wsp pathway. We predict that hyperbiofilm variants are early adaptations to infection and that interstrain interactions may influence bacterial burden and infection outcomes.


BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Perot Saelao ◽  
Michael Simone-Finstrom ◽  
Arian Avalos ◽  
Lelania Bilodeau ◽  
Robert Danka ◽  
...  

Abstract Background The population genetics of U.S. honey bee stocks remain poorly characterized despite the agricultural importance of Apis mellifera as the major crop pollinator. Commercial and research-based breeding programs have made significant improvements of favorable genetic traits (e.g. production and disease resistance). The variety of bees produced by artificial selection provides an opportunity to characterize the genetic diversity and regions of the genome undergoing selection in commonly managed stocks. Results Pooled sequencing of eight honey bee stocks found strong genetic similarity among six of the stocks. Two stocks, Pol-line and Hilo, showed significant differentiation likely due to their intense and largely closed breeding for resistance to the parasitic Varroa mite. Few variants were identified as being specific to any one stock, indicating potential admixture among the sequenced stocks. Juxtaposing the underlying genetic variation of stocks selected for disease- and parasite-resistance behavior, we identified genes and candidate regions putatively associated with resistance regulated by hygienic behavior. Conclusion This study provides important insights into the distinct genetic characteristics and population diversity of honey bee stocks used in the United States, and provides further evidence of high levels of admixture in commercially managed honey bee stocks. Furthermore, breeding efforts to enhance parasite resistance in honey bees may have created unique genetic profiles. Genomic regions of interest have been highlighted for potential future work related to developing genetic markers for selection of disease and parasite resistance traits. Due to the vast genomic similarities found among stocks in general, our findings suggest that additional data regarding gene expression, epigenetic and regulatory information are needed to more fully determine how stock phenotypic diversity is regulated.


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