scholarly journals ​Polygenic Trait

2019 ◽  
Author(s):  
Keyword(s):  
Polygenic Trait

scholarly journals Investigating mechanisms underlying genetic resistance to Salmon Rickettsial Syndrome in Atlantic salmon using RNA sequencing

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Carolina P. Moraleda ◽  
Diego Robledo ◽  
Alejandro P. Gutiérrez ◽  
Jorge del-Pozo ◽  
José M. Yáñez ◽  
...  
Keyword(s):  
Atlantic Salmon ◽  
Rna Sequencing ◽  
Host Resistance ◽  
Large Population ◽  
Genetic Resistance ◽  
Head Kidney ◽  
Breeding Values ◽  
Association Analyses ◽  
Polygenic Trait ◽  
Salmon Rickettsial Syndrome

Abstract Background Salmon Rickettsial Syndrome (SRS), caused by Piscirickettsia salmonis, is one of the primary causes of morbidity and mortality in Atlantic salmon aquaculture, particularly in Chile. Host resistance is a heritable trait, and functional genomic studies have highlighted genes and pathways important in the response of salmon to the bacteria. However, the functional mechanisms underpinning genetic resistance are not yet well understood. In the current study, a large population of salmon pre-smolts were challenged with P. salmonis, with mortality levels recorded and samples taken for genotyping. In parallel, head kidney and liver samples were taken from animals of the same population with high and low genomic breeding values for resistance, and used for RNA-Sequencing to compare their transcriptome profile both pre and post infection. Results A significant and moderate heritability (h2 = 0.43) was shown for the trait of binary survival. Genome-wide association analyses using 38 K imputed SNP genotypes across 2265 animals highlighted that resistance is a polygenic trait. Several thousand genes were identified as differentially expressed between controls and infected samples, and enriched pathways related to the host immune response were highlighted. In addition, several networks with significant correlation with SRS resistance breeding values were identified, suggesting their involvement in mediating genetic resistance. These included apoptosis, cytoskeletal organisation, and the inflammasome. Conclusions While resistance to SRS is a polygenic trait, this study has highlighted several relevant networks and genes that are likely to play a role in mediating genetic resistance. These genes may be future targets for functional studies, including genome editing, to further elucidate their role underpinning genetic variation in host resistance.

scholarly journals Quantity, Not Quality: Rapid Adaptation in a Polygenic Trait Proceeded Exclusively through Expression Differentiation

2017 ◽  
Vol 34 (12) ◽  
pp. 3099-3110 ◽  
Author(s):  
Mark J Margres ◽  
Kenneth P Wray ◽  
Alyssa T B Hassinger ◽  
Micaiah J Ward ◽  
James J McGivern ◽  
...  
Keyword(s):  
Rapid Adaptation ◽  
Polygenic Trait

scholarly journals Disentangling selection on genetically correlated polygenic traits using whole-genome genealogies

2020 ◽  
Author(s):  
Aaron J. Stern ◽  
Leo Speidel ◽  
Noah A. Zaitlen ◽  
Rasmus Nielsen
Keyword(s):  
Dna Sequence ◽  
Population Genetic ◽  
Sequence Data ◽  
Directional Selection ◽  
Likelihood Method ◽  
Correlated Response ◽  
Correlated Traits ◽  
Dna Sequence Data ◽  
Polygenic Traits ◽  
Polygenic Trait

AbstractWe present a full-likelihood method to estimate and quantify polygenic adaptation from contemporary DNA sequence data. The method combines population genetic DNA sequence data and GWAS summary statistics from up to thousands of nucleotide sites in a joint likelihood function to estimate the strength of transient directional selection acting on a polygenic trait. Through population genetic simulations of polygenic trait architectures and GWAS, we show that the method substantially improves power over current methods. We examine the robustness of the method under uncorrected GWAS stratification, uncertainty and ascertainment bias in the GWAS estimates of SNP effects, uncertainty in the identification of causal SNPs, allelic heterogeneity, negative selection, and low GWAS sample size. The method can quantify selection acting on correlated traits, fully controlling for pleiotropy even among traits with strong genetic correlation (|rg| = 80%; c.f. schizophrenia and bipolar disorder) while retaining high power to attribute selection to the causal trait. We apply the method to study 56 human polygenic traits for signs of recent adaptation. We find signals of directional selection on pigmentation (tanning, sunburn, hair, P=5.5e-15, 1.1e-11, 2.2e-6, respectively), life history traits (age at first birth, EduYears, P=2.5e-4, 2.6e-4, respectively), glycated hemoglobin (HbA1c, P=1.2e-3), bone mineral density (P=1.1e-3), and neuroticism (P=5.5e-3). We also conduct joint testing of 137 pairs of genetically correlated traits. We find evidence of widespread correlated response acting on these traits (2.6-fold enrichment over the null expectation, P=1.5e-7). We find that for several traits previously reported as adaptive, such as educational attainment and hair color, a significant proportion of the signal of selection on these traits can be attributed to correlated response, vs direct selection (P=2.9e-6, 1.7e-4, respectively). Lastly, our joint test uncovers antagonistic selection that has acted to increase type 2 diabetes (T2D) risk and decrease HbA1c (P=1.5e-5).

scholarly journals The effect of offspring number on the adaptation speed of a polygenic trait

2017 ◽  
Author(s):  
Markus Pfenninger
Keyword(s):  
Phenotypic Change ◽  
Phenotypic Variance ◽  
Genetic Trait ◽  
Hedging Strategy ◽  
Diploid Population ◽  
Offspring Number ◽  
Unpredictable Environments ◽  
Soft Selection ◽  
Polygenic Trait ◽  
Density Dependent Selection

There is increasing evidence that rapid phenotypic adaptation of quantitative traits is not uncommon in nature. However, the circumstances under which rapid adaptation of polygenic traits occurs are not yet understood. Building on previous concepts of soft selection, i.e. frequency and density dependent selection, I developed and tested the hypothesis that adaptation speed of a polygenic trait depends on the number of offspring per breeding pair in a randomly mating diploid population. Using individual based modelling on a range of offspring per parent (2-200) in populations of various size (100-10000 individuals), I could show that the by far largest proportion of variance (42%) was explained by the offspring number, regardless of genetic trait architecture (10-50 loci, different locus contribution distributions). In addition, it was possible to identify the majority of the responsible loci and account for even more of the observed phenotypic change with a moderate population size. The simulation results suggest that offspring numbers may a crucial factor for the adaptation speed of quantitative loci. Moreover, as large offspring numbers translates to a large phenotypic variance in the offspring of each parental pair, this genetic bet hedging strategy increases the chance to contribute to the next generation in unpredictable environments.

scholarly journals Polygenic adaptation: From sweeps to subtle frequency shifts

2018 ◽  
Author(s):  
Ilse Höllinger ◽  
Pleuni S Pennings ◽  
Joachim Hermisson
Keyword(s):  
Population Genetics ◽  
Allele Frequency ◽  
Mutation Rate ◽  
Quantitative Genetics ◽  
Large Set ◽  
Selective Sweeps ◽  
Genetic Redundancy ◽  
Small Frequency ◽  
Frequency Shifts ◽  
Polygenic Trait

1AbstractEvolutionary theory has produced two conflicting paradigms for the adaptation of a polygenic trait. While population genetics views adaptation as a sequence of selective sweeps at single loci underlying the trait, quantitative genetics posits a collective response, where phenotypic adaptation results from subtle allele frequency shifts at many loci. Yet, a synthesis of these views is largely missing and the population genetic factors that favor each scenario are not well understood. Here, we study the architecture of adaptation of a binary polygenic trait (such as resistance) with negative epistasis among the loci of its basis. The genetic structure of this trait allows for a full range of potential architectures of adaptation, ranging from sweeps to small frequency shifts. By combining computer simulations and a newly devised analytical framework based on Yule branching processes, we gain a detailed understanding of the adaptation dynamics for this trait. Our key analytical result is an expression for the joint distribution of mutant alleles at the end of the adaptive phase. This distribution characterizes the polygenic pattern of adaptation at the underlying genotype when phenotypic adaptation has been accomplished. We find that a single compound parameter, the population-scaled background mutation rate Θbg, explains the main differences among these patterns. For a focal locus, Θbg measures the mutation rate at all redundant loci in its genetic background that offer alternative ways for adaptation. For adaptation starting from mutation-selection-drift balance, we observe different patterns in three parameter regions. Adaptation proceeds by sweeps for small Θbg ≾ 0.1, while small polygenic allele frequency shifts require large Θbg ≿ 100. In the large intermediate regime, we observe a heterogeneous pattern of partial sweeps at several interacting loci.2Author summaryIt is still an open question how complex traits adapt to new selection pressures. While population genetics champions the search for selective sweeps, quantitative genetics proclaims adaptation via small concerted frequency shifts. To date the empirical evidence of clear sweep signals is more scarce than expected, while subtle shifts remain notoriously hard to detect. In the current study we develop a theoretical framework to predict the expected adaptive architecture of a simple polygenic trait, depending on parameters such as mutation rate, effective population size, size of the trait basis, and the available genetic variability at the onset of selection. For a population in mutation-selection-drift balance we find that adaptation proceeds via complete or partial sweeps for a large set of parameter values. We predict adaptation by small frequency shifts for two main cases. First, for traits with a large mutational target size and high levels of genetic redundancy among loci, and second if the starting frequencies of mutant alleles are more homogeneous than expected in mutation-selection-drift equilibrium, e.g. due to population structure or balancing selection.

scholarly journals Adult-Onset Alopecia Areata Is a Complex Polygenic Trait in the C3H/HeJ Mouse Model

2004 ◽  
Vol 123 (2) ◽  
pp. 294-297 ◽  
Author(s):  
John P. Sundberg ◽  
Kathleen A. Silva ◽  
Renhua Li ◽  
Gregory A. Cox ◽  
Lloyd E. King
Keyword(s):  
Mouse Model ◽  
Alopecia Areata ◽  
Adult Onset ◽  
Polygenic Trait

scholarly journals Intelligence: shared genetic basis between Mendelian disorders and a polygenic trait

2015 ◽  
Vol 23 (10) ◽  
pp. 1378-1383 ◽  
Author(s):  
Sanja Franić ◽  
Maria M Groen-Blokhuis ◽  
Conor V Dolan ◽  
Mathijs V Kattenberg ◽  
René Pool ◽  
...  
Keyword(s):  
Genetic Basis ◽  
Mendelian Disorders ◽  
Polygenic Trait ◽  
Shared Genetic

scholarly journals GlobAl Distribution of GEnetic Traits (GADGET) web server: polygenic trait scores worldwide

2018 ◽  
Vol 46 (W1) ◽  
pp. W121-W126 ◽  
Author(s):  
Aroon T Chande ◽  
Lu Wang ◽  
Lavanya Rishishwar ◽  
Andrew B Conley ◽  
Emily T Norris ◽  
...  
Keyword(s):  
Web Server ◽  
Global Distribution ◽  
Genetic Traits ◽  
Polygenic Trait
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