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37 results for “Genetic Load”
Epistatic selection on a selfish Segregation Distorter supergene: drive, recombination, and genetic load
<p>Meiotic drive supergenes are complexes of alleles at linked loci that together subvert Mendelian segregation resulting in preferential transmission. In males, the most common mechanism of drive involves the disruption of sperm bearing one of a pair of alternative alleles. While at least two loci are important for male drive- the driver and the target- linked modifiers can enhance drive, creating selection pressure to suppress recombination. In this work, we investigate the evolution and genomic consequences of an autosomal, multilocus, male meiotic drive system, Segregation Distorter (SD) in the fruit fly, Drosophila melanogaster. In African populations, the predominant SD chromosome variant, SD-Mal, is characterized by two overlapping, paracentric inversions on chromosome arm 2R and nearly perfect (~100%) transmission. We study the SD-Mal system in detail, exploring its components, chromosomal structure, and evolutionary history. Our findings reveal a recent chromosome-scale selective sweep mediated by strong epistatic selection for haplotypes carrying Sd, the main driving allele, and one or more factors within the double inversion. While most SD-Mal chromosomes are homozygous lethal, SD-Mal haplotypes can recombine with other, complementing haplotypes via crossing over, and with wildtype chromosomes via gene conversion. SD-Mal chromosomes have nevertheless accumulated lethal mutations, excess non-synonymous mutations, and excess transposable element insertions. Therefore, SD-Mal haplotypes evolve as a small, semi-isolated subpopulation with a history of strong selection. These results may explain the evolutionary turnover of SD haplotypes in different populations around the world, and have implications for supergene evolution broadly.</p>
Deep-sequencing of viral genomes from treatment-naive HIV-infected persons shows positive association between intrahost genetic diversity and viral load
<p><strong><span>Background:</span></strong><span> Infection with human immunodeficiency virus type 1 (HIV) typically results from transmission of a small and genetically uniform viral population. Following transmission, the virus population becomes more diverse because of recombination and acquired mutations through genetic drift and selection. Viral intrahost genetic diversity remains a major obstacle to the cure of HIV; however, there is a disagreement whether intrahost viral genetic diversification associates positively or negatively with disease progression and progression markers. Viral load is a key progression marker and understanding its relationship to viral intrahost genetic diversity could help design future strategies for HIV monitoring and treatment.</span></p> <p><span><strong>Methods:</strong> </span><span>We analyzed deep-sequenced viral genomes from 2,650 treatment-naive HIV-infected persons to measure the intrahost genetic diversity of 2,447 genomic codon positions as calculated by Shannon entropy. We tested for associations between viral load (VL) and amino acid (AA) entropy accounting for sex, age, race, duration of infection, and HIV population structure.</span></p> <p><strong><span>Results:</span></strong><span><strong> </strong>We confirmed that the intrahost genetic diversity is highest in the <em>env</em> gene. Furthermore, we showed that mean Shannon entropy is significantly associated with VL, especially in infections of >24 months duration. We identified 16 significant associations between VL (p-value<2.0x10<sup>-5</sup>) and Shannon entropy at AA positions which in our association analysis explained 13% of the variance in VL.</span></p> <p><strong><span>Conclusions: </span></strong><span>Our results elucidate that viral intrahost genetic diversity is associated with VL and could be used as a better disease progression marker than HIV consensus sequence variants, especially in infections of longer duration. We emphasize that viral intrahost diversity should be considered when studying viral genomes and infection outcomes.</span></p>
Load Shifting Optimization with Genetic Algorithms for Energy Cost Minimization in Households - Case Study Data2
<p>The case study of this dataset uses real household data, representing five days from 0h00 to 23h59. This dataset uses a period of 15 minutes for all loads execution time and energy data. The case study considers twenty unique houses that can have up to five different shiftable appliances, each executing three process cycles.<br> <br> File Description:</p> <ul> <li>Case_Studies_Data-BAU_and_Load_Shifting - Excel containing appliances energy profile, load execution preferences, BAU consumption, and houses' data</li> <li>Houses_Input_Output_JSONs_and_Statistics - Zip containing the input and output files from the proposed system, as well as their corresponding schedule statistics</li> </ul>
Load Shifting Optimization with Genetic Algorithms for Energy Cost Minimization in Households - Case Study Data
<p>The case study of this dataset uses real household data, representing five days from 0h00 to 23h59. This dataset uses a period of 15 minutes for all loads execution time and energy data. The case study considers twenty unique houses that can have up to five different shiftable appliances, each executing three process cycles.<br> <br> File Description:</p> <ul> <li>Case_Studies_Data-BAU_and_Load_Shifting - Excel containing appliances energy profile, load execution preferences, BAU consumption, and other house data</li> <li>Houses_Input_JSONs - Zip containing the input files, from each house, for the proposed system</li> </ul>
From high masked to high realized genetic load in inbred Scandinavian wolves
<p><span>When new mutations arise at functional sites they are more likely to impair than improve fitness. If not removed by purifying selection, such deleterious mutations will generate a genetic load that can have negative fitness effects in small populations and increase the risk of extinction. This is relevant for the highly inbred Scandinavian wolf (<em>Canis</em> <em>lupus</em>) population, founded by only three wolves in the 1980s and suffering from inbreeding depression. We used functional annotation and evolutionary conservation scores to study deleterious variation in a total of 209 genomes from both the Scandinavian and neighboring wolf populations in northern Europe. The masked load (deleterious mutations in heterozygote state) was highest in Russia and Finland with deleterious alleles segregating at lower frequency than neutral variation. Genetic drift in the Scandinavian population led to the loss of ancestral alleles, fixation of deleterious variants and a significant increase in the per-individual realized load (deleterious mutations in homozygote state; an increase by 45% in protein-coding genes) over five generations of inbreeding. Arrival of immigrants gave a temporary genetic rescue effect with ancestral alleles re-entering the population and thereby shifting deleterious alleles from homozygous into heterozygote genotypes. However, in the absence of permanent connectivity to Finnish and Russian populations, inbreeding has then again led to the exposure of deleterious mutations. These observations provide genome-wide insight into the magnitude of genetic load and genetic rescue at the molecular level, and in relation to population history. They emphasize the importance of securing gene flow in the management of endangered populations.<br></span></p>
The relative strength of selection on modifiers of genetic architecture under migration load
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Structural genomic variation in the inbred Scandinavian wolf population contributes to the realized genetic load but is positively affected by immigration
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Epistatic selection on a selfish Segregation Distorter supergene: drive, recombination, and genetic load
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Deep-sequencing of viral genomes from treatment-naive HIV-infected persons shows positive association between intrahost genetic diversity and viral load
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From high masked to high realized genetic load in inbred Scandinavian wolves
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Genomic evidence that a sexually selected trait captures genome-wide variation and facilitates the purging of genetic load
<p><span>The evolution of costly traits like deer antlers and peacock trains, which drove the formation of Darwinian sexual selection theory, has been hypothesised to both reflect and affect patterns of genetic variance across the genome, but direct tests are missing. Here, we used an evolve and re-sequence approach to reveal patterns of genome-wide diversity associated with the expression of a sexually-selected weapon that is dimorphic among males of the bulb mite,</span> <em>Rhizoglyphus robini</em><span>. Populations selected for the weapon </span>showed reduced genome-wide diversity compared to populations selected against the weapon, particularly in terms of the number of segregating non-synonymous positions, indicating enhanced purifying selection. <span>This increased purifying selection reduced inbreeding depression, but outbred female fitness did not improve, possibly because any benefits were offset by increased sexual antagonism. </span>The majority of single nucleotide polymorphisms (SNPs) that consistently diverged in response to selection were initially rare and overrepresented in exons, and enriched in regions under balancing or relaxed selection, suggesting they are likely moderately deleterious variants. These diverged SNPs were scattered across the genome, <span>further demonstrating that selection for or against the weapon and the associated changes to the mating system can both capture and influence genome-wide variation. </span></p>
Give and take: Effects of genetic admixture on mutation load in endangered Florida panthers
<p>Genetic admixture is a biological event inherent to genetic rescue programs aimed at the long-term conservation of endangered wildlife. Although the success of such programs can be measured by the increase in genetic diversity and fitness of subsequent admixed individuals, predictions supporting admixture costs to fitness due to the introduction of novel deleterious alleles are necessary. Here, we analyzed nonsynonymous variation from conserved genes to quantify and compare levels of mutation load (i.e., proportion of deleterious alleles and genotypes carrying these alleles) among endangered Florida panthers and non-endangered Texas pumas. Specifically, we used canonical (i.e., non-admixed) Florida panthers, Texas pumas, and F<sub>1</sub> (canonical Florida x Texas) panthers dating from a genetic rescue program and Everglades National Park panthers with Central American ancestry resulting from an earlier admixture event. We found neither genetic drift nor selection significantly reduced overall proportions of deleterious alleles in the severely bottlenecked canonical Florida panthers. Nevertheless, the deleterious alleles identified were distributed into a disproportionately high number of homozygous genotypes due to close inbreeding in this group. Conversely, admixed Florida panthers (either with Texas or Central American ancestry) presented reduced levels of homozygous genotypes carrying deleterious alleles but increased levels of heterozygous genotypes carrying these variants relative to canonical Florida panthers. Although admixture is likely to alleviate the load of standing deleterious variation present in homozygous genotypes, our results suggest introduced novel deleterious alleles (temporarily present in heterozygous state) in genetically rescued populations could potentially be expressed in subsequent generations if their effective sizes remain small.</p>
Summary data for plots in: Eco-evolutionary extinction and recolonization dynamics reduce genetic load and increase time to extinction in highly inbred populations
<p>Understanding how genetic and ecological effects can interact to shape genetic loads within and across local populations is key to understanding ongoing persistence of systems that should otherwise be susceptible to extinction through mutational meltdown. Classic theory predicts short persistence times for metapopulations comprising small local populations with low connectivity, due to accumulation of deleterious mutations. Yet, some such systems have persisted over evolutionary time, implying the existence of mechanisms that allow metapopulations to avoid mutational meltdown. We first hypothesize a mechanism by which the combination of stochasticity in the numbers and types of mutations arising locally (genetic stochasticity), resulting in local extinction and recolonization through evolving dispersal, facilitates metapopulation persistence. We then test this mechanism using a spatially and genetically explicit individual-based model. We show that genetic stochasticity in highly structured metapopulations can result in local extinctions, which can favour increased dispersal, thus allowing recolonization of empty habitat patches. This causes fluctuations in metapopulation size and transient gene flow, which reduces genetic load and increases metapopulation persistence over evolutionary time. Our suggested mechanism and simulation results provide an explanation for the conundrum presented by the continued persistence of highly structured populations with inbreeding mating systems that occur in diverse taxa.</p>
Data from: Genomes of Galápagos mockingbirds reveal the impact of island size and past demography on inbreeding and genetic load in contemporary populations
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Give and take: Effects of genetic admixture on mutation load in endangered Florida panthers
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Summary data for plots in: Eco-evolutionary extinction and recolonization dynamics reduce genetic load and increase time to extinction in highly inbred populations
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Genomic evidence that a sexually selected trait captures genome-wide variation and facilitates the purging of genetic load
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Data from: The power of evolutionary rescue is constrained by genetic load
Extinction risk of small isolated populations in changing environments can be reduced by rapid adaptation and subsequent growth to larger, less vulnerable sizes. Whether this process, called evolutionary rescue, is able to reduce extinction risk and sustain population growth over multiple generations is largely unknown. To understand the consequences of adaptive evolution as well as maladaptive processes in small isolated populations, we subjected experimental Tribolium castaneum populations founded with 10 or 40 individuals to novel environments, one more favorable, and one resource poor, and either allowed evolution, or constrained it by replacing individuals one-for-one each generation from a non-adapting large population to minimize both adaptive and non-adaptive evolutionary processes. Replacement individuals spent one generation in the target novel environment before use to standardize effects due to the parental environment. After 8 generations we mixed a subset of surviving populations to facilitate admixture, allowing us to estimate drift load by comparing performance of mixed to unmixed groups. Evolving populations had reduced extinction rates, and increased population sizes in the first four to five generations compared to populations where evolution was constrained. Performance of evolving populations subsequently declined. Admixture restored their performance, indicating high drift load that may have overwhelmed the beneficial effects of adaptation in evolving populations. Our results indicate that evolution may quickly reduce extinction risk and increase population sizes, but suggest that relying solely on adaptation from standing genetic variation may not provide long-term benefits to small isolated populations of diploid sexual species, and that active management facilitating gene flow may be necessary for longer-term persistence.
Data from: Demographic expansion and genetic load of the halophyte model plant Eutrema salsugineum
Eutrema salsugineum is a widely distributed species, which provide a good model to study long-distance dispersal and accumulation of deleterious mutations. Based on population genomic data, we clarified demographic history of E. salsugineum and showed how deleterious alleles accumulated.
Genetic of Response to Acute Saline Load Test in Hypertension (Naload)
ClinicalTrials.gov study NCT04625569. IPD Sharing: UNDECIDED. Countries: 1. Publications: 4.
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