scholarly journals Uniparental inheritance promotes adaptive evolution in cytoplasmic genomes

2016 ◽  
Author(s):  
Joshua R. Christie ◽  
Madeleine Beekman
Keyword(s):  
Computational Model ◽  
Adaptive Evolution ◽  
Maternal Inheritance ◽  
Host Cells ◽  
Uniparental Inheritance ◽  
Selective Sweeps ◽  
Clonal Interference ◽  
Genetic Hitchhiking ◽  
Mode Of Reproduction ◽  
Unique Biology

1AbstractEukaryotes carry numerous asexual cytoplasmic genomes (mitochondria and plastids). Lacking recombination, asexual genomes should theoretically suffer from impaired adaptive evolution. Yet, empirical evidence indicates that cytoplasmic genomes experience higher levels of adaptive evolution than predicted by theory. In this study, we use a computational model to show that the unique biology of cytoplasmic genomes—specifically their organization into host cells and their uniparental (maternal) inheritance—enable them to undergo effective adaptive evolution. Uniparental inheritance of cytoplasmic genomes decreases competition between different beneficial substitutions (clonal interference), promoting the accumulation of beneficial substitutions. Uniparental inheritance also facilitates selection against deleterious cytoplasmic substitutions, slowing Muller’s ratchet. In addition, uniparental inheritance generally reduces genetic hitchhiking of deleterious substitutions during selective sweeps. Overall, uniparental inheritance promotes adaptive evolution by increasing the level of beneficial substitutions relative to deleterious substitutions. When we assume that cytoplasmic genome inheritance is biparental, decreasing the number of genomes transmitted during gametogenesis (bottleneck) aids adaptive evolution. Nevertheless, adaptive evolution is always more efficient when inheritance is uniparental. Our findings explain empirical observations that cytoplasmic genomes—despite their asexual mode of reproduction—can readily undergo adaptive evolution.

scholarly journals Adaptation, Clonal Interference, and Frequency-Dependent Interactions in a Long-Term Evolution Experiment with Escherichia coli

2015 ◽  
Author(s):  
Rohan Maddamsetti ◽  
Richard E. Lenski ◽  
Jeffrey E. Barrick
Keyword(s):  
Escherichia Coli ◽  
Frequency Dependence ◽  
Evolutionary Dynamics ◽  
Selective Sweeps ◽  
Clonal Interference ◽  
Beneficial Mutations ◽  
Frequency Dependent ◽  
Evolution Experiment ◽  
History Of

Twelve replicate populations of Escherichia coli have been evolving in the laboratory for more than 25 years and 60,000 generations. We analyzed bacteria from whole-population samples frozen every 500 generations through 20,000 generations for one well-studied population, called Ara???1. By tracking 42 known mutations in these samples, we reconstructed the history of this population???s genotypic evolution over this period. The evolutionary dynamics of Ara???1 show strong evidence of selective sweeps as well as clonal interference between competing lineages bearing different beneficial mutations. In some cases, sets of several mutations approached fixation simultaneously, often conveying no information about their order of origination; we present several possible explanations for the existence of these mutational cohorts. Against a backdrop of rapid selective sweeps both earlier and later, we found that two clades coexisted for over 6000 generations before one drove the other extinct. In that time, at least nine mutations arose in the clade that prevailed. We found evidence that the clades evolved a frequency-dependent interaction, which prevented the competitive exclusion of either clade, but which eventually collapsed as beneficial mutations accumulated in the clade that prevailed. Clonal interference and frequency dependence can occur even in the simplest microbial populations. Furthermore, frequency dependence may generate dynamics that extend the period of coexistence that would otherwise be sustained by clonal interference alone.

scholarly journals A Computational Model for the Evaluation of Complement System Regulation under Homeostasis, Disease, and Drug Intervention

2017 ◽  
Author(s):  
Nehemiah Zewde ◽  
Dimitrios Morikis
Keyword(s):  
Computational Model ◽  
Complement System ◽  
Complement Activation ◽  
Late Stage ◽  
Inflammatory Diseases ◽  
Early Stage ◽  
Host Cells ◽  
Patient Specific ◽  
Complement Dysregulation ◽  
The Complement System

HighlightsComputational model describing dynamics of complement system activation pathwaysComplement dysregulation leads to deviation from homeostasis and to inflammatory diseasesModel identifies biomarkers to quantify the effects of complement dysregulationKnown drugs restore impaired dynamics of complement biomarkers under dysregulationDisease-specific models are suitable for diagnosis and patient-specific drug treatmentAbstractThe complement system is a part of innate immunity that rapidly removes invading pathogens and impaired host-cells. Activation of the complement system is balanced under homeostasis by regulators that protect healthy host-cells. Impairment of complement regulators tilts the balance, favoring activation and propagation that leads to inflammatory diseases. The most potent regulator of the complement system is Factor H (FH), and its impairment induces improper complement activation that leads to inflammatory diseases, such as atypical hemolytic uremic syndrome and age related macular degeneration. To understand the dynamics involved in the pivotal balance between activation and regulation, we have developed a comprehensive computational model of the alternative and classical pathways of the complement system. The model is composed of 290 ordinary differential equations with 142 kinetic parameters that describe the state of complement system under homeostasis and disorder through FH impairment. We have evaluated the state of the system by generating concentration-time profiles for the biomarkers C3, C3a-desArg, C5, C5a-desArg, Factor B (FB), Ba, Bb, and fC5b-9 that are influenced by complement dysregulation. We show that FH-mediated disorder induces substantial levels of complement activation compared to homeostasis, by generating reduced levels of C3 and FB, and to a lesser extent C5, and elevated levels of C3a-desArg, Ba, Bb, C5a-desArg, and fC5b-9. These trends are consistent with clinically observed biomarkers associated with complement-mediated diseases. Furthermore, we introduced therapy states by modeling known drugs of the complement system, a compstatin variant (C3 inhibitor) and eculizumab (a C5 inhibitor). Compstatin demonstrates strong restorative effects for early-stage biomarkers, such as C3a-desArg, FB, Ba, and Bb, and milder restorative effects for late-stage biomarkers, such as C5a-desArg and fC5b-9, whereas eculizumab has strong restorative effects on late-stage biomarkers, and negligible effects on early-stage biomarkers. These results highlight the need for patient-specific therapies that target early complement activation at the C3 level, or late-stage propagation of the terminal cascade at the C5 level, depending on the specific FH-mediated disease and the manifestations of a patient’s genetic profile in complement regulatory function.

scholarly journals Selective sweeps of mitochondrial DNA can drive the evolution of uniparental inheritance

Evolution ◽  
2017 ◽  
Vol 71 (8) ◽  
pp. 2090-2099 ◽  
Author(s):  
Joshua R. Christie ◽  
Madeleine Beekman
Keyword(s):  
Mitochondrial Dna ◽  
Uniparental Inheritance ◽  
Selective Sweeps

scholarly journals The effects on neutral variability of recurrent selective sweeps and background selection

2018 ◽  
Author(s):  
José Luis Campos ◽  
Brian Charlesworth
Keyword(s):  
Adaptive Evolution ◽  
Selective Sweep ◽  
Crossing Over ◽  
Background Selection ◽  
Selective Sweeps ◽  
Population Genomic ◽  
Approximate Integral ◽  
Theoretical Predictions ◽  
Site Diversity ◽  
Coalescent Time

ABSTRACTLevels of variability and rates of adaptive evolution may be affected by hitchhiking, the effect of selection on evolution at linked sites. Hitchhiking can be caused either by selective sweeps or by background selection, involving the spread of new favorable alleles or the elimination of deleterious mutations, respectively. Recent analyses of population genomic data have fitted models where both these processes act simultaneously, in order to infer the parameters of selection. Here, we investigate the consequences of relaxing a key assumption of some of these studies – that the time occupied by a selective sweep is negligible compared with the neutral coalescent time. We derive a new expression for the expected level of neutral variability in the presence of recurrent selective sweeps and background selection. We also derive approximate integral expressions for the effects of recurrent selective sweeps. The accuracy of the theoretical predictions was tested against multilocus simulations, with selection, recombination and mutation parameters that are realistic for Drosophila melanogaster. In the presence of crossing over, there is approximate agreement between the theoretical and simulation results. We show that the observed relations between the rate of crossing over and the level of synonymous site diversity and rate of adaptive evolution in Drosophila are probably mainly caused by background selection, whereas selective sweeps and population size changes are needed to produce the observed distortions of the site frequency spectrum.

scholarly journals Pervasive genetic hitchhiking and clonal interference in forty evolving yeast populations

Nature ◽  
2013 ◽  
Vol 500 (7464) ◽  
pp. 571-574 ◽  
Author(s):  
Gregory I. Lang ◽  
Daniel P. Rice ◽  
Mark J. Hickman ◽  
Erica Sodergren ◽  
George M. Weinstock ◽  
...  
Keyword(s):  
Clonal Interference ◽  
Genetic Hitchhiking

scholarly journals Host-Virus Arms Races Drive Elevated Adaptive Evolution in Viral Receptors

2020 ◽  
Vol 94 (16) ◽  
Author(s):  
Wenqiang Wang ◽  
Huayao Zhao ◽  
Guan-Zhu Han
Keyword(s):  
Positive Selection ◽  
Local Adaptation ◽  
Adaptive Evolution ◽  
Negative Selection ◽  
Host Cells ◽  
Human Populations ◽  
Arms Races ◽  
Selection Pressures ◽  
Selection For ◽  
Viral Receptors

ABSTRACT Viral receptors are the cell surface proteins that are hijacked by viruses to initialize their infections. Viral receptors are subject to two conflicting directional forces, namely, negative selection due to functional constraints and positive selection due to host-virus arms races. It remains largely obscure whether negative pleiotropy limits the rate of adaptation in viral receptors. Here, we perform evolutionary analyses of 96 viral receptor genes in primates and find that 41 out of 96 viral receptors experienced adaptive evolution. Many positively selected residues in viral receptors are located at the virus-receptor interfaces. Compared with control proteins, viral receptors exhibit significantly elevated rate of adaptation. Further analyses of genetic polymorphisms in human populations reveal signals of positive selection and balancing selection for 53 and 5 viral receptors, respectively. Moreover, we find that 49 viral receptors experienced different selection pressures in different human populations, indicating that viruses represent an important driver of local adaptation in humans. Our findings suggest that diverse viruses, many of which have not been known to infect nonhuman primates, have maintained antagonistic associations with primates for millions of years, and the host-virus conflicts drive accelerated adaptive evolution in viral receptors. IMPORTANCE Viruses hijack cellular proteins, termed viral receptors, to assist their entry into host cells. While viral receptors experience negative selection to maintain their normal functions, they also undergo positive selection due to an everlasting evolutionary arms race between viruses and hosts. A complete picture on how viral receptors evolve under two conflicting forces is still lacking. In this study, we systematically analyzed the evolution of 96 viral receptors in primates and human populations. We found around half of viral receptors underwent adaptive evolution and exhibit significantly elevated rates of adaptation compared to control genes in primates. We also found signals of past natural selection for 58 viral receptors in human populations. Interestingly, 49 viral receptors experienced different selection pressures in different human populations, indicating that viruses represent an important driver of local adaptation in humans. Our results suggest that host-virus arms races drive accelerated adaptive evolution in viral receptors.

scholarly journals A naturally heteroplasmic clam provides clues about the effects of genetic bottleneck on paternal mtDNA

2021 ◽  
Author(s):  
Mariangela Iannello ◽  
Stefano Bettinazzi ◽  
Sophie Breton ◽  
Fabrizio Ghiselli ◽  
Liliana Milani
Keyword(s):  
Maternal Inheritance ◽  
Ruditapes Philippinarum ◽  
Uniparental Inheritance ◽  
Single Individual ◽  
Doubly Uniparental Inheritance ◽  
Large Variability ◽  
Unique System ◽  
Multiple Copies ◽  
First Time ◽  
Different Tissues

Abstract Mitochondrial DNA (mtDNA) is present in multiple copies within an organism. Since these copies are not identical, a single individual carries a heterogeneous population of mtDNAs, a condition known as heteroplasmy. Several factors play a role in the dynamics of the within-organism mtDNA population: among them genetic bottlenecks, selection, and strictly maternal inheritance are known to shape the levels of heteroplasmy across mtDNAs. In Metazoa, the only evolutionarily stable exception to the strictly maternal inheritance of mitochondria is the doubly uniparental inheritance (DUI), reported in 100+ bivalve species. In DUI species there are two highly divergent mtDNA lineages, one inherited through oocyte mitochondria (F-type) and the other through sperm mitochondria (M-type). Having both parents contributing to the mtDNA pool of the progeny makes DUI a unique system to study the dynamics of mtDNA populations. Since in bivalves the spermatozoon has few mitochondria (4-5), M-type mtDNA faces a tight bottleneck during embryo segregation, one of the narrowest mitochondrial bottlenecks investigated so far. Here, we analyzed the F- and M-type mtDNA variability within individuals of the DUI species Ruditapes philippinarum, and we investigated for the first time the effects of such a narrow bottleneck affecting mtDNA populations. As a potential consequence of this narrow bottleneck, the M-type mtDNA shows a large variability in different tissues, a condition so pronounced that it leads to genotypes from different tissues of the same individual not to cluster together. We believe such results may help understanding the effect of low population size on mtDNA bottleneck.

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