Latest recommendations
Id | Title | Authors | Abstract | Picture | Thematic fields | Recommender▲ | Reviewers | Submission date | |
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18 Dec 2017
Co-evolution of virulence and immunosuppression in multiple infectionsTsukushi Kamiya, Nicole Mideo, Samuel Alizon 10.1101/149211Two parasites, virulence and immunosuppression: how does the whole thing evolve?Recommended by Sara Magalhaes based on reviews by 2 anonymous reviewersHow parasite virulence evolves is arguably the most important question in both the applied and fundamental study of host-parasite interactions. Typically, this research area has been progressing through the formalization of the problem via mathematical modelling. This is because the question is a complex one, as virulence is both affected and affects several aspects of the host-parasite interaction. Moreover, the evolution of virulence is a problem in which ecology (epidemiology) and evolution (changes in trait values through time) are tightly intertwined, generating what is now known as eco-evolutionary dynamics. Therefore, intuition is not sufficient to address how virulence may evolve. References [1] Anderson RM and May RM. 1982. Coevolution of hosts and parasites. Parasitology, 1982. 85: 411–426. doi: 10.1017/S0031182000055360 [2] Kamiya T, Mideo N and Alizon S. 2017. Coevolution of virulence and immunosuppression in multiple infections. bioRxiv, ver. 7 peer-reviewed by PCI Evol Biol, 149211. doi: 10.1101/139147 | Co-evolution of virulence and immunosuppression in multiple infections | Tsukushi Kamiya, Nicole Mideo, Samuel Alizon | Many components of the host-parasite interaction have been shown to affect the way virulence, that is parasite induced harm to the host, evolves. However, co-evolution of multiple traits is often neglected. We explore how an immunosuppressive mech... | Evolutionary Applications, Evolutionary Dynamics, Evolutionary Ecology, Evolutionary Epidemiology, Evolutionary Theory | Sara Magalhaes | 2017-06-13 16:49:45 | View | ||
06 Jun 2019
Multi-model inference of non-random mating from an information theoretic approachAntonio Carvajal-Rodríguez https://doi.org/10.1101/305730Tell me who you mate with, I’ll tell you what’s going onRecommended by Sara Magalhaes and Alexandre Courtiol based on reviews by Alexandre Courtiol and 2 anonymous reviewersThe study of sexual selection goes as far as Darwin himself. Since then, elaborate theories concerning both intra- and inter-sexual sexual have been developed, and elegant experiments have been designed to test this body of theory. It may thus come as a surprise that the community is still debating on the correct way to measure simple components of sexual selection, such as the Bateman gradient (i.e., the covariance between the number of matings and the number of offspring)[1,2], or to quantify complex behaviours such as mate choice (the non-random choice of individuals with particular characters as mates)[3,4] and their consequences. References [1] Bateman, A. J. (1948). Intra-sexual selection in Drosophila. Heredity, 2(3), 349-368. doi: 10.1038/hdy.1948.21 | Multi-model inference of non-random mating from an information theoretic approach | Antonio Carvajal-Rodríguez | <p>Non-random mating has a significant impact on the evolution of organisms. Here, I developed a modelling framework for discrete traits (with any number of phenotypes) to explore different models connecting the non-random mating causes (mate comp... | Evolutionary Ecology, Evolutionary Theory, Sexual Selection | Sara Magalhaes | 2019-02-08 19:24:03 | View | ||
18 May 2018
Modularity of genes involved in local adaptation to climate despite physical linkageKatie E. Lotterhos, Sam Yeaman, Jon Degner, Sally Aitken, Kathryn Hodgins https://doi.org/10.1101/202481Differential effect of genes in diverse environments, their role in local adaptation and the interference between genes that are physically linkedRecommended by Sebastian Ernesto Ramos-Onsins based on reviews by Tanja Pyhäjärvi and 1 anonymous reviewerThe genome of eukaryotic species is a complex structure that experience many different interactions within itself and with the surrounding environment. The genetic architecture of a phenotype (that is, the set of genetic elements affecting a trait of the organism) plays a fundamental role in understanding the adaptation process of a species to, for example, different climate environments, or to its interaction with other species. Thus, it is fundamental to study the different aspects of the genetic architecture of the species and its relationship with its surronding environment. Aspects such as modularity (the number of genetic units and the degree to which each unit is affecting a trait of the organism), pleiotropy (the number of different effects that a genetic unit can have on an organism) or linkage (the degree of association between the different genetic units) are essential to understand the genetic architecture and to interpret the effects of selection on the genome. Indeed, the knowledge of the different aspects of the genetic architecture could clarify whether genes are affected by multiple aspects of the environment or, on the contrary, are affected by only specific aspects [1,2]. The work performed by Lotterhos et al. [3] sought to understand the genetic architecture of the adaptation to different environments in lodgepole pine (Pinus contorta), considering as candidate SNPs those previously detected as a result of its extreme association patterns to different environmental variables or to extreme population differentiation. This consideration is very important because the study is only relevant if the studied markers are under the effect of selection. Otherwise, the genetic architecture of the adaptation to different environments would be masked by other (neutral) kind of associations that would be difficult to interpret [4,5]. In order to understand the relationship between genetic architecture and adaptation, it is relevant to detect the association networks of the candidate SNPs with climate variables (a way to measure modularity) and if these SNPs (and loci) are affected by single or multiple environments (a way to measure pleiotropy). The authors used co-association networks, an innovative approach in this field, to analyse the interaction between the environmental information and the genetic polymorphism of each individual. This methodology is more appropriate than other multivariate methods - such as analysis based on principal components - because it is possible to cluster SNPs based on associations with similar environmental variables. In this sense, the co-association networks allowed to both study the genetic and physical linkage between different co-associations modules but also to compare two different models of evolution: a Modular environmental response architecture (specific genes are affected by specific aspects of the environment) or a Universal pleiotropic environmental response architecture (all genes are affected by all aspects of the environment). The representation of different correlations between allelic frequency and environmental factors (named galaxy biplots) are especially informative to understand the effect of the different clusters on specific aspects of the environment (for example, the co-association network ‘Aridity’ shows strong associations with hot/wet versus cold/dry environments). The analysis performed by Lotterhos et al. [3], although it has some unavoidable limitations (e.g., only extreme candidate SNPs are selected, limiting the results to the stronger effects; the genetic and physical map is incomplete in this species), includes relevant results and also implements new methodologies in the field. To highlight some of them: the preponderance of a Modular environmental response architecture (evolution in separated modules), the detection of physical linkage among SNPs that are co-associated with different aspects of the environment (which was unexpected a priori), the implementation of co-association networks and galaxy biplots to see the effect of modularity and pleiotropy on different aspects of environment. Finally, this work contains remarkable introductory Figures and Tables explaining unambiguously the main concepts [6] included in this study. This work can be treated as a starting point for many other future studies in the field. References [1] Hancock AM, Brachi B, Faure N, Horton MW, Jarymowycz LB, Sperone FG, Toomajian C, Roux F & Bergelson J. 2011. Adaptation to climate across the Arabidopsis thaliana genome. Science 334: 83–86. doi: 10.1126/science.1209244 | Modularity of genes involved in local adaptation to climate despite physical linkage | Katie E. Lotterhos, Sam Yeaman, Jon Degner, Sally Aitken, Kathryn Hodgins | <p>Background: Physical linkage among genes shaped by different sources of selection is a fundamental aspect of genetic architecture. Theory predicts that evolution in complex environments selects for modular genetic architectures and high recombi... | Adaptation, Bioinformatics & Computational Biology, Genome Evolution | Sebastian Ernesto Ramos-Onsins | 2017-10-15 19:21:57 | View | ||
20 Nov 2019
Distribution of iridescent colours in hummingbird communities results from the interplay between selection for camouflage and communicationHugo Gruson, Marianne Elias, Juan L. Parra, Christine Andraud, Serge Berthier, Claire Doutrelant, Doris Gomez https://doi.org/10.1101/586362Feathers iridescence sheds light on the assembly rules of humingbirds communitiesRecommended by Sébastien Lavergne based on reviews by 2 anonymous reviewersEcology needs rules stipulating how species distributions and ecological communities should be assembled along environmental gradients, but few rules have yet emerged in the ecological literature. The search of ecogeographical rules governing the spatial variation of birds colours has recently known an upsurge of interest in the litterature [1]. Most studies have, however, looked at pigmentary colours and not structural colours (e.g. iridescence), although it is know that color perception by animals (both birds and their predators) can be strongly influenced by light diffraction causing iridescence patterns on feathers. References [1] Delhey, K. (2019). A review of Gloger’s rule, an ecogeographical rule of colour: definitions, interpretations and evidence. Biological Reviews, 94(4), 1294–1316. doi: 10.1111/brv.12503 | Distribution of iridescent colours in hummingbird communities results from the interplay between selection for camouflage and communication | Hugo Gruson, Marianne Elias, Juan L. Parra, Christine Andraud, Serge Berthier, Claire Doutrelant, Doris Gomez | <p>Identification errors between closely related, co-occurring, species may lead to misdirected social interactions such as costly interbreeding or misdirected aggression. This selects for divergence in traits involved in species identification am... | Evolutionary Ecology, Macroevolution, Phylogeography & Biogeography, Sexual Selection, Species interactions | Sébastien Lavergne | 2019-03-29 17:23:20 | View | ||
18 Nov 2022
Fitness costs and benefits in response to artificial artesunate selection in PlasmodiumVilla M, Berthomieu A, Rivero A https://doi.org/10.1101/2022.01.28.478164The importance of understanding fitness costs associated with drug resistance throughout the life cycle of malaria parasitesRecommended by Silvie Huijben based on reviews by Sarah Reece and Marianna SzucsAntimalarial resistance is a major hurdle to malaria eradication efforts. The spread of drug resistance follows basic evolutionary principles, with competitive interactions between resistant and susceptible malaria strains being central to the fitness of resistant parasites. These competitive interactions can be used to design resistance management strategies, whereby a fitness cost of resistant parasites can be exploited through maintaining competitive suppression of the more fit drug-susceptible parasites. This can potentially be achieved using lower drug dosages or lower frequency of drug treatments. This approach has been demonstrated to work empirically in a rodent malaria model [1,2] and has been demonstrated to have clinical success in cancer treatments [3]. However, these resistance management approaches assume a fitness cost of the resistant pathogen, and, in the case of malaria parasites in general, and for artemisinin resistant parasites in particular, there is limited information on the presence of such fitness cost. The best suggestive evidence for the presence of fitness costs comes from the discontinuation of the use of the drug, which, in the case of chloroquine, was followed by a gradual drop in resistance frequency over the following decade [see e.g. 4,5]. However, with artemisinin derivative drugs still in use, alternative ways to study the presence of fitness costs need to be undertaken. References [1] Huijben S, Bell AS, Sim DG, Tomasello D, Mideo N, Day T, et al. 2013. Aggressive chemotherapy and the selection of drug resistant pathogens. PLoS Pathog. 9(9): e1003578. https://doi.org/10.1371/journal.ppat.1003578 [5] Mharakurwa S, Matsena-Zingoni Z, Mudare N, Matimba C, Gara TX, Makuwaza A, et al. 2021. Steep rebound of chloroquine-sensitive Plasmodium falciparum in Zimbabwe. J Infect Dis. 223(2): 306-9. https://doi.org/10.1093/infdis/jiaa368 | Fitness costs and benefits in response to artificial artesunate selection in Plasmodium | Villa M, Berthomieu A, Rivero A | <p style="text-align: justify;">Drug resistance is a major issue in the control of malaria. Mutations linked to drug resistance often target key metabolic pathways and are therefore expected to be associated with biological costs. The spread of dr... | Evolutionary Applications, Life History | Silvie Huijben | 2022-01-31 13:01:16 | View | ||
06 Mar 2023
Extrinsic mortality and senescence: a guide for the perplexedCharlotte de Vries, Matthias Galipaud, Hanna Kokko https://doi.org/10.1101/2022.01.27.478060Getting old gracefully, and risk of dying before getting there: a new guide to theory on extrinsic mortality and senescenceRecommended by Sinead English and Shinichi Nakagawa based on reviews by Nicole Walasek and 1 anonymous reviewerWhy is there such variation across species and populations in the rate at which individuals show wear and tear as they get older? Several compelling theoretical explanations have been developed on the conditions under which selection allows for or prevents senescence; a notable one being that proposed by George C Williams in 1957 based on the idea of antagonistic pleiotropy (Williams, 1957). One of the testable predictions of this theory is that, in populations where adults experience higher mortality, senescence is expected to be faster. This is one of the most influential predictions of the paper, being intuitive (when individuals are less likely to survive to later age classes, we expect weakened selection on traits that would avoid senescence in these classes), and fitting with ‘live fast, die young’ life history framing. As such, it has been widely incorporated into how we think about the evolution of senescence and has received considerable support in comparative studies across species and populations. However, it would be misleading to sit back at this point and think we have ‘solved’ the problem of understanding variation in senescence, and how this is linked with mortality. It turns out that the Williams 1957 paper is hotly contested by theoreticians: for the past 30 years – with increasing focus in the last 4 years – a growing body of models and opinion pieces have proposed flaws in the paper itself and in how it has been interpreted (Abrams, 1993; André and Rousset, 2020; Day and Abrams, 2020; Moorad et al., 2019). Central to several of these critiques is that explicit consideration of density dependence (not considered in Williams’ original paper) changes the conditions under which his predictions hold. A new preprint by de Vries, Gallipaud and Kokko brings further clarity to such critiques of the original paper (Vries et al., 2023). Beyond just continuing the tradition of critiquing Williams’ prediction, however, de Vries et al. provide a clear guide that is accessible to non-theoreticians about the issues with William’s prediction, and the way in which density dependence and how it operates can change when we expect senescence to occur. Rather than reiterate their points here, we suggest a close reading of the paper itself, along with an excellent overview of the paper in a recent blog by Daniel Nettle (Nettle, 2022). In brief, the paper starts by synthesizing earlier theoretical and empirical studies on the topic and presenting a very simple model to highlight how – in the absence of density dependence – Williams’ prediction does not hold because of the unregulated population growth, which is necessarily higher when there is low mortality. As a result, for a lineage with low mortality, any fitness advantage of placing offspring into the lineage later (i.e. selection for reduced senescence) is exactly cancelled out by the fact that earlier-produced offspring have higher fitness returns. They then present a more complex framework, which incorporates realistic mortality distributions, trade-offs between survival and reproduction, and use a series of 10 scenarios of density dependence (and whether this acts on survival or fecundity, and also whether it depends on a threshold or stochastic, or exerts continuing pressure on the trait) to explore selection on fitness-associated traits with age depending on extrinsic mortality. This then generates a range of results for when the Williams prediction holds, when there is no link between mortality and senescence, and when there is an ‘anti-Williams’ result – i.e., where senescence is slower when there is a high mortality. As has been shown in earlier studies, density dependence and how it operates matters, and Williams’ prediction holds most when density dependence affects juvenile age classes (in their model, when adults are less likely to produce them – i.e. there is density dependence on fecundity; or when there is less recruitment into the adult population due to, for example, competition among juveniles). So, perhaps we are now at a point where we can lay to rest the debate on the issues specifically with Williams’ original paper, and instead consider more broadly the key factors to measure when predicting patterns of senescence, and what is tangible for empiricists to quantify in their studies. Here, de Vries et al. provide some helpful insights both into the limitations of their approach and what modelling should be done moving forward, and into how we can link existing studies (for example comparing senescence among populations with varying predation pressure) to the theoretical predictions. At the heart of the latter is understanding the mechanism of density-dependent regulation – does it affect survival or fecundity, which age classes are most sensitive, and how do key traits depend on density? – and this is often difficult to measure in field studies. And from all this we can learn that even very intuitive and extensively discussed concepts in biology do not always have as firm theoretical underpinnings as assumed, and – as should not be surprising – biology is complex and rather than one clear pattern being predicted, this can depend on a multitude of factors. REFERENCES Abrams PA (1993) Does increased mortality favor the evolution of more rapid senescence? Evolution, 47, 877–887. https://doi.org/10.1111/j.1558-5646.1993.tb01241.x André J-B, Rousset F (2020) Does extrinsic mortality accelerate the pace of life? A bare-bones approach. Evolution and Human Behavior, 41, 486–492. https://doi.org/10.1016/j.evolhumbehav.2020.03.002 Day T, Abrams PA (2020) Density Dependence, Senescence, and Williams’ Hypothesis. Trends in Ecology & Evolution, 35, 300–302. https://doi.org/10.1016/j.tree.2019.11.005 Moorad J, Promislow D, Silvertown J (2019) Evolutionary Ecology of Senescence and a Reassessment of Williams’ ‘Extrinsic Mortality’ Hypothesis. Trends in Ecology & Evolution, 34, 519–530. https://doi.org/10.1016/j.tree.2019.02.006 Nettle AD (2022) Live fast and die young (maybe). https://www.danielnettle.org.uk/2022/02/18/live-fast-and-die-young-maybe/ (accessed 2.27.23). de Vries C, Galipaud M, Kokko H (2023) Extrinsic mortality and senescence: a guide for the perplexed. bioRxiv, 2022.01.27.478060, ver. 5 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2022.01.27.478060 Williams GC (1957) Pleiotropy, natural selection, and the evolution of senescence. Evolution, 11, 398–411. https://doi.org/10.1111/j.1558-5646.1957.tb02911.x | Extrinsic mortality and senescence: a guide for the perplexed | Charlotte de Vries, Matthias Galipaud, Hanna Kokko | <p style="text-align: justify;">Do environments or species traits that lower the mortality of individuals create selection for delaying senescence? Reading the literature creates an impression that mathematically oriented biologists cannot agree o... | Evolutionary Dynamics, Evolutionary Ecology, Evolutionary Theory, Life History | Sinead English | 2022-08-26 14:30:16 | View | ||
03 Apr 2017
Things softly attained are long retained: Dissecting the Impacts of Selection Regimes on Polymorphism Maintenance in Experimental Spatially Heterogeneous EnvironmentsRomain Gallet, Rémy Froissart, Virginie Ravigné https://doi.org/10.1101/100743Experimental test of the conditions of maintenance of polymorphism under hard and soft selectionRecommended by Stephanie Bedhomme based on reviews by Joachim Hermisson and 2 anonymous reviewers
Theoretical work, initiated by Levene (1953) [1] and Dempster (1955) [2], suggests that within a given environment, the way populations are regulated and contribute to the next generation is a key factor for the maintenance of local adaptation polymorphism. In this theoretical context, hard selection describes the situation where the genetic composition of each population affects its contribution to the next generation whereas soft selection describes the case where the contribution of each population is fixed, whatever its genetic composition. Soft selection is able to maintain polymorphism, whereas hard selection invariably leads to the fixation of one of the alleles. Although the specific conditions (e.g. of migration between populations or drift level) in which this prediction holds have been studied in details by theoreticians, experimental tests have mainly failed, usually leading to the conclusion that the allele frequency dynamics was driven by other mechanisms in the experimental systems and conditions used. Gallet, Froissart and Ravigné [3] have set up a bacterial experimental system which allowed them to convincingly demonstrate that soft selection generates the conditions for polymorphism maintenance when hard selection does not, everything else being equal. The key ingredients of their experimental system are (1) the possibility to accurately produce hard and soft selection regimes when daily transferring the populations and (2) the ability to establish artificial well-characterized reproducible trade-offs. To do so, they used two genotypes resisting each one to one antibiotic and combined, across habitats, low antibiotic doses and difference in medium productivity. The experimental approach contains two complementary parts: the first one is looking at changes in the frequencies of two genotypes, initially introduced at around 50% each, over a small number of generations (ca 40) in different environments and selection regimes (soft/hard) and the second one is convincingly showing polymorphism protection by establishing that in soft selection regimes, the lowest fitness genotype is not eliminated even when introduced at low frequency. In this manuscript, a key point is the dialog between theoretical and experimental approaches. The experiments have been thought and designed to be as close as possible to the situations analysed in theoretical work. For example, the experimental polymorphism protection test (experiment 2) closely matches the equivalent analysis classically performed in theoretical approaches. This close fit between theory and experiment is clearly a strength of this study. This said, the experimental system allowing them to realise this close match also has some limitations. For example, changes in allele frequencies could only be monitored over a quite low number of generations because a longer time-scale would have allowed the contribution of de novo mutations and the likely emergence of a generalist genotype resisting to both antibiotics used to generate the local adaptation trade-offs. These limitations, as well as the actual significance of the experimental tests, are discussed in deep details in the manuscript. References [1] Levene H. 1953. Genetic equilibrium when more than one niche is available. American Naturalist 87: 331–333. doi: 10.1086/281792 [2] Dempster ER. 1955. Maintenance of genetic heterogeneity. Cold Spring Harbor Symposia on Quantitative Biology. 20: 25–32. doi: 10.1101/SQB.1955.020.01.005 [3] Gallet R, Froissart R, Ravigné V. 2017. Things softly attained are long retained: dissecting the impacts of selection regimes on polymorphism maintenance in experimental spatially heterogeneous environments. bioRxiv 100743; doi: 10.1101/100743 | Things softly attained are long retained: Dissecting the Impacts of Selection Regimes on Polymorphism Maintenance in Experimental Spatially Heterogeneous Environments | Romain Gallet, Rémy Froissart, Virginie Ravigné | <p>Predicting and managing contemporary adaption requires a proper understanding of the determinants of genetic variation. Spatial heterogeneity of the environment may stably maintain polymorphism when habitat contribution to the next generation c... | Adaptation, Evolutionary Theory | Stephanie Bedhomme | 2017-01-17 11:06:21 | View | ||
31 Jan 2018
Identifying drivers of parallel evolution: A regression model approachSusan F Bailey, Qianyun Guo, Thomas Bataillon https://doi.org/10.1101/118695A new statistical tool to identify the determinant of parallel evolutionRecommended by Stephanie Bedhomme based on reviews by Bastien Boussau and 1 anonymous reviewerIn experimental evolution followed by whole genome resequencing, parallel evolution, defined as the increase in frequency of identical changes in independent populations adapting to the same environment, is often considered as the product of similar selection pressures and the parallel changes are interpreted as adaptive. References [1] Bailey SF, Guo Q and Bataillon T (2018) Identifying drivers of parallel evolution: A regression model approach. bioRxiv 118695, ver. 4 peer-reviewed by Peer Community In Evolutionary Biology. doi: 10.1101/118695 [2] Lang GI, Rice DP, Hickman, MJ, Sodergren E, Weinstock GM, Botstein D, and Desai MM (2013) Pervasive genetic hitchhiking and clonal interference in forty evolving yeast populations. Nature 500: 571–574. doi: 10.1038/nature12344 | Identifying drivers of parallel evolution: A regression model approach | Susan F Bailey, Qianyun Guo, Thomas Bataillon | <p>This preprint has been reviewed and recommended by Peer Community In Evolutionary Biology (http://dx.doi.org/10.24072/pci.evolbiol.100045). Parallel evolution, defined as identical changes arising in independent populations, is often attributed... | Experimental Evolution, Molecular Evolution | Stephanie Bedhomme | 2017-03-22 14:54:48 | View | ||
05 Nov 2020
A genomic amplification affecting a carboxylesterase gene cluster confers organophosphate resistance in the mosquito Aedes aegypti: from genomic characterization to high-throughput field detectionJulien Cattel, Chloé Haberkorn, Fréderic Laporte, Thierry Gaude, Tristan Cumer, Julien Renaud, Ian W. Sutherland, Jeffrey C. Hertz, Jean-Marc Bonneville, Victor Arnaud, Camille Noûs, Bénédicte Fustec, Sébastien Boyer, Sébastien Marcombe, Jean-Philippe David https://doi.org/10.1101/2020.06.08.139741Identification of a gene cluster amplification associated with organophosphate insecticide resistance: from the diversity of the resistance allele complex to an efficient field detection assayRecommended by Stephanie Bedhomme based on reviews by Diego Ayala and 2 anonymous reviewersThe emergence and spread of insecticide resistance compromises the efficiency of insecticides as prevention tool against the transmission of insect-transmitted diseases (Moyes et al. 2017). In this context, the understanding of the genetic mechanisms of resistance and the way resistant alleles spread in insect populations is necessary and important to envision resistance management policies. A common and important mechanism of insecticide resistance is gene amplification and in particular amplification of insecticide detoxification genes, which leads to the overexpression of these genes (Bass & Field, 2011). Cattel and coauthors (2020) adopt a combination of experimental approaches to study the role of gene amplification in resistance to organophosphate insecticides in the mosquito Aedes aegypti and its occurrence in populations of South East Asia and to develop a molecular test to track resistance alleles. References Bass C, Field LM (2011) Gene amplification and insecticide resistance. Pest Management Science, 67, 886–890. https://doi.org/10.1002/ps.2189 | A genomic amplification affecting a carboxylesterase gene cluster confers organophosphate resistance in the mosquito Aedes aegypti: from genomic characterization to high-throughput field detection | Julien Cattel, Chloé Haberkorn, Fréderic Laporte, Thierry Gaude, Tristan Cumer, Julien Renaud, Ian W. Sutherland, Jeffrey C. Hertz, Jean-Marc Bonneville, Victor Arnaud, Camille Noûs, Bénédicte Fustec, Sébastien Boyer, Sébastien Marcombe, Jean-Phil... | <p>By altering gene expression and creating paralogs, genomic amplifications represent a key component of short-term adaptive processes. In insects, the use of insecticides can select gene amplifications causing an increased expression of detoxifi... | Adaptation, Evolutionary Applications, Experimental Evolution, Genome Evolution, Molecular Evolution | Stephanie Bedhomme | 2020-06-09 13:27:18 | View | ||
12 Nov 2020
Limits and Convergence properties of the Sequentially Markovian CoalescentThibaut Sellinger, Diala Abu Awad, Aurélien Tellier https://doi.org/10.1101/2020.07.23.217091Review and Assessment of Performance of Genomic Inference Methods based on the Sequentially Markovian CoalescentRecommended by Stephan Schiffels based on reviews by 3 anonymous reviewersThe human genome not only encodes for biological functions and for what makes us human, it also encodes the population history of our ancestors. Changes in past population sizes, for example, affect the distribution of times to the most recent common ancestor (tMRCA) of genomic segments, which in turn can be inferred by sophisticated modelling along the genome. References [1] Li, H., and Durbin, R. (2011). Inference of human population history from individual whole-genome sequences. Nature, 475(7357), 493-496. doi: https://doi.org/10.1038/nature10231 | Limits and Convergence properties of the Sequentially Markovian Coalescent | Thibaut Sellinger, Diala Abu Awad, Aurélien Tellier | <p>Many methods based on the Sequentially Markovian Coalescent (SMC) have been and are being developed. These methods make use of genome sequence data to uncover population demographic history. More recently, new methods have extended the original... | Population Genetics / Genomics | Stephan Schiffels | Anonymous | 2020-07-25 10:54:48 | View |
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