| 1. |
- Alvarez-Castro, Jose M., et al.
(författare)
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How to perform meaningful estimates of genetic effects
- 2008
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Ingår i: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 4:5, s. e1000062-
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Tidskriftsartikel (refereegranskat)abstract
- Although the genotype-phenotype map plays a central role both in Quantitative and Evolutionary Genetics, the formalization of a completely general and satisfactory model of genetic effects, particularly accounting for epistasis, remains a theoretical challenge. Here, we use a two-locus genetic system in simulated populations with epistasis to show the convenience of using a recently developed model, NOIA, to perform estimates of genetic effects and the decomposition of the genetic variance that are orthogonal even under deviations from the Hardy-Weinberg proportions. We develop the theory for how to use this model in interval mapping of quantitative trait loci using Halley-Knott regressions, and we analyze a real data set to illustrate the advantage of using this approach in practice. In this example, we show that departures from the Hardy-Weinberg proportions that are expected by sampling alone substantially alter the orthogonal estimates of genetic effects when other statistical models, like F-2 or G2A, are used instead of NOIA. Finally, for the first time from real data, we provide estimates of functional genetic effects as sets of effects of natural allele substitutions in a particular genotype, which enriches the debate on the interpretation of genetic effects as implemented both in functional and in statistical models. We also discuss further implementations leading to a completely general genotype-phenotype map.
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| 2. |
- Alvarez-Castro, Jose, et al.
(författare)
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Modelling of genetic interactions improves prediction of hybrid patterns : a case study in domestic fowl
- 2012
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Ingår i: Genetical Research. - 0016-6723 .- 1469-5073. ; 94:5, s. 255-266
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Tidskriftsartikel (refereegranskat)abstract
- Summary A major challenge in complex trait genetics is to unravel how multiple loci and environmental factors together cause phenotypic diversity. Both first (F1) and second (F2) generation hybrids often display phenotypes that deviate from what is expected under intermediate inheritance. We have here studied two chicken F2 populations generated by crossing divergent chicken lines to assess how epistatic loci, identified in earlier quantitative trait locus (QTL) studies, contribute to hybrid deviations from the mid-parent phenotype. Empirical evidence suggests that the average phenotypes of the intercross birds tend to be lower than the midpoint between the parental means in both crosses. Our results confirm that epistatic interactions, despite a relatively small contribution to the phenotypic variance, play an important role in the deviation of hybrid phenotypes from the mid-parent values (i.e. multi-locus hybrid genotypes lead to lower rather than higher body weights). To a lesser extent, dominance also appears to contribute to the mid-parent deviation, at least in one of the crosses. This observation coincides with the hypothesis that hybridization tends to break up co-adapted gene complexes, i.e. generate Bateson-Dobzhansky-Muller incompatibilities.
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| 3. |
- Chevin, Luis Miguel, et al.
(författare)
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Using phenotypic plasticity to understand the structure and evolution of the genotype–phenotype map
- 2021
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Ingår i: Genetica. - : Springer Science and Business Media LLC. - 0016-6707 .- 1573-6857.
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Tidskriftsartikel (refereegranskat)abstract
- Deciphering the genotype–phenotype map necessitates relating variation at the genetic level to variation at the phenotypic level. This endeavour is inherently limited by the availability of standing genetic variation, the rate of spontaneous mutation to novo genetic variants, and possible biases associated with induced mutagenesis. An interesting alternative is to instead rely on the environment as a source of variation. Many phenotypic traits change plastically in response to the environment, and these changes are generally underlain by changes in gene expression. Relating gene expression plasticity to the phenotypic plasticity of more integrated organismal traits thus provides useful information about which genes influence the development and expression of which traits, even in the absence of genetic variation. We here appraise the prospects and limits of such an environment-for-gene substitution for investigating the genotype–phenotype map. We review models of gene regulatory networks, and discuss the different ways in which they can incorporate the environment to mechanistically model phenotypic plasticity and its evolution. We suggest that substantial progress can be made in deciphering this genotype–environment–phenotype map, by connecting theory on gene regulatory network to empirical patterns of gene co-expression, and by more explicitly relating gene expression to the expression and development of phenotypes, both theoretically and empirically.
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| 4. |
- Le Rouzic, Arnaud, et al.
(författare)
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Dissection of the genetic architecture of body weight in chicken reveals the impact of epistasis on domestication traits
- 2008
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Ingår i: Genetics. - : Oxford University Press (OUP). - 0016-6731 .- 1943-2631. ; 179:3, s. 1591-1599
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Tidskriftsartikel (refereegranskat)abstract
- In this contribution, we study the genetic mechanisms leading to differences in the observed growth patterns of domesticated White Leghorn chickens and their wild ancestor the red jungle fowl. An epistatic QTL analysis for several body-weight measures from hatch to adulthood confirms earlier findings that polymorphisms at > , 15 loci contribute to body-weight determination in an F-2 intercross between these populations and that many loci are involved in complex genetic interactions. Here, we use a new genetic model to decompose the genetic effects of this multilocus epistatic genetic network. The results show how the functional modeling of genetic effects provides new insights into how genetic interactions in a large set of loci jointly contribute to phenotypic expression. By exploring the functional effects of QTL allels, we show that some alleles can display temporal shifts in the expression of genetic effects due to their dependencies on the genetic background. Our results demonstrate that the effects of many genes are dependent on genetic interactions with other loci and how their involvement in the domestication process relies on these interactions.
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| 5. |
- Le Rouzic, Arnaud, et al.
(författare)
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Evolutionary potential of hidden genetic variation
- 2008
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Ingår i: Trends in Ecology & Evolution. - : Elsevier BV. - 0169-5347 .- 1872-8383. ; 23:1, s. 33-37
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Forskningsöversikt (refereegranskat)abstract
- The ability of a population to respond to natural or artificial selection pressures is determined by the genetic architecture of the selected trait. It is now widely acknowledged that a substantial part of genetic variability can be buffered or released as the result of complex genetic interactions. However, the impact of hidden genetic diversity on phenotypic evolution is still not clear. Here, we argue that a common term to describe the impact of hidden genetic variation on phenotypic change is needed and will help to provide new insights into the contribution of different components of genetic architectures to the evolvability of a character. We introduce the 'genetic charge' concept, to describe how the architecture of a trait can be 'charged' with potential for evolutionary change that can later be 'discharged' in response to selection.
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| 6. |
- Le Rouzic, Arnaud, et al.
(författare)
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Evolutionary Time-Series Analysis Reveals the Signature of Frequency-Dependent Selection on a Female Mating Polymorphism
- 2015
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Ingår i: American Naturalist. - : University of Chicago Press. - 0003-0147 .- 1537-5323. ; 185:6, s. 182-196
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Tidskriftsartikel (refereegranskat)abstract
- A major challenge in evolutionary biology is understanding how stochastic and deterministic factors interact and influence macroevolutionary dynamics in natural populations. One classical approach is to record frequency changes of heritable and visible genetic polymorphisms over multiple generations. Here, we combined this approach with a maximum likelihood-based population-genetic model with the aim of understanding and quantifying the evolutionary processes operating on a female mating polymorphism in the blue-tailed damselfly Ischnura elegans. Previous studies on this color-polymorphic species have suggested that males form a search image for females, which leads to excessive mating harassment of common female morphs. We analyzed a large temporally and spatially replicated data set of between-generation morph frequency changes in I. elegans. Morph frequencies were more stable than expected from genetic drift alone, suggesting the presence of selection toward a stable equilibrium that prevents local loss or fixation of morphs. This can be interpreted as the signature of negative frequency-dependent selection maintaining the phenotypic stasis and genetic diversity in these populations. Our novel analytical approach allows the estimation of the strength of frequency-dependent selection from the morph frequency fluctuations around their inferred long-term equilibria. This approach can be extended and applied to other polymorphic organisms for which time-series data across multiple generations are available.
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| 7. |
- Le Rouzic, Arnaud, et al.
(författare)
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Phenotypic evolution from genetic polymorphisms in a radial network architecture
- 2007
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Ingår i: BMC Biology. - : Springer Science and Business Media LLC. - 1741-7007. ; 5, s. 50-
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Tidskriftsartikel (refereegranskat)abstract
- Background: The genetic architecture of a quantitative trait influences the phenotypic response to natural or artificial selection. One of the main objectives of genetic mapping studies is to identify the genetic factors underlying complex traits and understand how they contribute to phenotypic expression. Presently, we are good at identifying and locating individual loci with large effects, but there is a void in describing more complex genetic architectures. Although large networks of connected genes have been reported, there is an almost complete lack of information on how polymorphisms in these networks contribute to phenotypic variation and change. To date, most of our understanding comes from theoretical, model-based studies, and it remains difficult to assess how realistic their conclusions are as they lack empirical support. Results: A previous study provided evidence that nearly half of the difference in eight-week body weight between two divergently selected lines of chickens was a result of four loci organized in a 'radial' network (one central locus interacting with three 'radial' loci that, in turn, only interacted with the central locus). Here, we study the relationship between phenotypic change and genetic polymorphism in this empirically detected network. We use a model-free approach to study, through individual-based simulations, the dynamic properties of this polymorphic and epistatic genetic architecture. The study provides new insights to how epistasis can modify the selection response, buffer and reveal effects of major loci leading to a progressive release of genetic variation. We also illustrate the difficulty of predicting genetic architecture from observed selection response, and discuss mechanisms that might lead to misleading conclusions on underlying genetic architectures from quantitative trait locus (QTL) experiments in selected populations. Conclusion: Considering both molecular (QTL) and phenotypic (selection response) data, as suggested in this work, provides additional insights into the genetic mechanisms involved in the response to selection. Such dissection of genetic architectures and in-depth studies of their ability to contribute to short-or long-term selection response represents an important step towards a better understanding of the genetic bases of complex traits and, consequently, of the evolutionary properties of populations.
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