Latest recommendations
| Id | Title | Authors | Abstract | Picture | Thematic fields | Recommender | Reviewers▼ | Submission date | |
|---|---|---|---|---|---|---|---|---|---|
23 Jan 2020
A novel workflow to improve multi-locus genotyping of wildlife species: an experimental set-up with a known model systemImproving the reliability of genotyping of multigene families in non-model organismsRecommended by François Rousset based on reviews by Sebastian Ernesto Ramos-Onsins, Helena Westerdahl and Thomas BigotThe reliability of published scientific papers has been the topic of much recent discussion, notably in the biomedical sciences [1]. Although small sample size is regularly pointed as one of the culprits, big data can also be a concern. The advent of high-throughput sequencing, and the processing of sequence data by opaque bioinformatics workflows, mean that sequences with often high error rates are produced, and that exact but slow analyses are not feasible. References [1] Ioannidis, J. P. A, Greenland, S., Hlatky, M. A., Khoury, M. J., Macleod, M. R., Moher, D., Schulz, K. F. and Tibshirani, R. (2014) Increasing value and reducing waste in research design, conduct, and analysis. The Lancet, 383, 166-175. doi: 10.1016/S0140-6736(13)62227-8 | A novel workflow to improve multi-locus genotyping of wildlife species: an experimental set-up with a known model system | Gillingham, Mark A. F., Montero, B. Karina, Wilhelm, Kerstin, Grudzus, Kara, Sommer, Simone and Santos, Pablo S. C. | <p>Genotyping novel complex multigene systems is particularly challenging in non-model organisms. Target primers frequently amplify simultaneously multiple loci leading to high PCR and sequencing artefacts such as chimeras and allele amplification... | | Bioinformatics & Computational Biology, Evolutionary Ecology, Genome Evolution, Molecular Evolution | François Rousset | Helena Westerdahl, Sebastian Ernesto Ramos-Onsins, Paul J. McMurdie , Arnaud Estoup, Vincent Segura, Jacek Radwan , Torbjørn Rognes , William Stutz , Kevin Vanneste , Thomas Bigot, Jill A. Hollenbach , Wieslaw Babik , Marie-Christin... | 2019-05-15 17:30:44 | |
30 Jun 2023
How do monomorphic bacteria evolve? The Mycobacterium tuberculosis complex and the awkward population genetics of extreme clonalityHow the tubercle bacillus got its genome: modernising, modelling, and making sense of the stories we tellRecommended by B. Jesse Shapiro based on reviews by 2 anonymous reviewersIn this instructive review, Stritt and Gagneux offer a balanced perspective on the evolutionary forces shaping Mycobacterium tuberculosis and make the case that our instinct for storytelling be balanced with quantitative models. M. tuberculosis is perhaps the best-known clonal bacterial pathogen – evolving largely in the absence of horizontal gene transfer. Its genome is full of puzzling patterns, including much higher GC content than most intracellular pathogens (which suggests efficient selection to resist AT-skewed mutational bias) but a very high ratio of nonsynonymous to synonymous substitution rates (dN/dS ~ 0.5, typically interpreted as weak selection against deleterious amino acid changes). The authors offer alternative explanations for these patterns, framing the question: is M. tuberculosis evolution shaped mainly by drift or by efficient selection? They propose that this question can only be answered by accounting for the pathogen’s extreme clonality. A clonal lifestyle can have its advantages, for example when adaptations must arise in a particular order (Kondrashov and Kondrashov 2001). An important disadvantage highlighted by the authors are linkage effects: without recombination to shuffle them up, beneficial mutations are linked to deleterious mutations in the same genome (hitchhiking) and purging deleterious mutations also purges neutral diversity across the genome (background selection). The authors propose the latter – efficient purifying selection and strong linkage – as an explanation for the low genetic diversity observed in M. tuberculosis. This is of course not exclusive of other related explanations, such as clonal interference (Gerrish and Lenski 1998). They also champion the use of forward evolutionary simulations (Haller and Messer 2019) to model the interplay between selection, recombination, and demography as a powerful alternative to traditional backward coalescent models. At times, Stritt and Gagneux are pessimistic about our existing methods – arguing that dN/dS and homoplasies “tell us little about the frequency and strength of selection.” Even though I favour a more optimistic view, I fully agree that our traditional population genetic metrics are sensitive to a slew of different deviations from a standard neutral evolution model and must be interpreted with caution. As I and others have argued, the extent of recombination (measured as the amount of linkage in a genome) is a key factor in determining how best to test for natural selection (Shapiro et al. 2009) and to conduct genotype-phenotype association studies (Chen and Shapiro 2021) in microbes. While this article is focused on the well-studied M. tuberculosis complex, there are many parallels with other clonal bacteria, including pathogens and symbionts. Whatever your favourite bug, we must all be careful to make sure the stories we tell about them are not “just so tales” but are supported, to the extent possible, by data and quantitative models. References Chen, Peter E., and B. Jesse Shapiro. 2021. "Classic Genome-Wide Association Methods Are Unlikely to Identify Causal Variants in Strongly Clonal Microbial Populations." bioRxiv. Stritt, C., Gagneux, S. (2023). How do monomorphic bacteria evolve? The Mycobacterium tuberculosis complex and the awkward population genetics of extreme clonality. EcoEvoRxiv, ver.3 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.32942/X2GW2P | How do monomorphic bacteria evolve? The *Mycobacterium tuberculosis* complex and the awkward population genetics of extreme clonality | Christoph Stritt, Sebastien Gagneux | <p style="text-align: justify;">Exchange of genetic material through sexual reproduction or horizontal gene transfer is ubiquitous in nature. Among the few outliers that rarely recombine and mainly evolve by <em>de novo</em> mutation are a group o... | | Evolutionary Dynamics, Genome Evolution, Molecular Evolution, Population Genetics / Genomics, Reproduction and Sex | B. Jesse Shapiro | Gonçalo Themudo | 2022-12-16 13:41:53 | |
29 Sep 2022
How many sirtuin genes are out there? evolution of sirtuin genes in vertebrates with a description of a new family memberMaking sense of vertebrate sirtuin genesRecommended by Frédéric Delsuc based on reviews by Filipe Castro, Nicolas Leurs and 1 anonymous reviewerSirtuin proteins are class III histone deacetylases that are involved in a variety of fundamental biological functions mostly related to aging. These proteins are located in different subcellular compartments and are associated with different biological functions such as metabolic regulation, stress response, and cell cycle control [1]. In mammals, the sirtuin gene family is composed of seven paralogs (SIRT1-7) grouped into four classes [2]. Due to their involvement in maintaining cell cycle integrity, sirtuins have been studied as a way to understand fundamental mechanisms governing longevity [1]. Indeed, the downregulation of sirtuin genes with aging seems to explain much of the pathophysiology that accumulates with aging [3]. Biomedical studies have thus explored the potential therapeutic implications of sirtuins [4] but whether they can effectively be used as molecular targets for the treatment of human diseases remains to be demonstrated [1]. Despite this biomedical interest and some phylogenetic analyses of sirtuin paralogs mostly conducted in mammals, a comprehensive evolutionary analysis of the sirtuin gene family at the scale of vertebrates was still lacking. In this preprint, Opazo and collaborators [5] took advantage of the increasing availability of whole-genome sequences for species representing all main groups of vertebrates to unravel the evolution of the sirtuin gene family. To do so, they undertook a phylogenomic approach in its original sense aimed at improving functional predictions by evolutionary analysis [6] in order to inventory the full vertebrate sirtuin gene repertoire and reconstruct its precise duplication history. Harvesting genomic databases, they extracted all predicted sirtuin proteins and performed phylogenetic analyses based on probabilistic inference methods. Maximum likelihood and Bayesian analyses resulted in well-resolved and congruent phylogenetic trees dividing vertebrate sirtuin genes into three major clades. These analyses also revealed an additional eighth paralog that was previously overlooked because of its restricted phyletic distribution. This newly identified sirtuin family member (named SIRT8) was recovered with unambiguous statistical support as a sister-group to the SIRT3 clade. Comparative genomic analyses based on conserved gene synteny confirmed that SIRT8 was present in all sampled non-amniote vertebrate genomes (cartilaginous fish, bony fish, coelacanth, lungfish, and amphibians) except cyclostomes. SIRT8 has thus most likely been lost in the last common ancestor of amniotes (mammals, reptiles, and birds). Discovery of such previously unknown genes in vertebrates is not completely surprising given the plethora of high-quality genomes now available. However, this study highlights the importance of considering a broad taxonomic sampling to infer evolutionary patterns of gene families that have been mostly studied in mammals because of their potential importance for human biology. Based on its phylogenetic position as closely related to SIRT3 within class I, it could be predicted that the newly identified SIRT8 paralog likely has a deacetylase activity and is probably located in mitochondria. To test these evolutionary predictions, Opazo and collaborators [5] conducted further bioinformatics analyses and functional experiments using the elephant shark (Callorhinchus milii) as a model species. RNAseq expression data were analyzed to determine tissue-specific transcription of sirtuin genes in vertebrates, including SIRT8 found to be mainly expressed in the ovary, which suggests a potential role in biological processes associated with reproduction. The elephant shark SIRT8 protein sequence was used with other vertebrates for comparative analyses of protein structure modeling and subcellular localization prediction both pointing to a probable mitochondrial localization. The protein localization and its function were further characterized by immunolocalization in transfected cells, and enzymatic and functional assays, which all confirmed the prediction that SIRT8 proteins are targeted to the mitochondria and have deacetylase activity. The extensive experimental efforts made in this study to shed light on the function of this newly discovered gene are both rare and highly commendable. Overall, this work by Opazo and collaborators [5] provides a comprehensive phylogenomic study of the sirtuin gene family in vertebrates based on detailed evolutionary analyses using state-of-the-art phylogenetic reconstruction methods. It also illustrates the power of adopting an integrative comparative approach supplementing the reconstruction of the duplication history of the gene family with complementary functional experiments in order to elucidate the function of the newly discovered SIRT8 family member. These results provide a reference phylogenetic framework for the evolution of sirtuin genes and the further functional characterization of the eight vertebrate paralogs with potential relevance for understanding the cellular biology of aging and its associated diseases in human. References [1] Vassilopoulos A, Fritz KS, Petersen DR, Gius D (2011) The human sirtuin family: Evolutionary divergences and functions. Human Genomics, 5, 485. https://doi.org/10.1186/1479-7364-5-5-485 [2] Yamamoto H, Schoonjans K, Auwerx J (2007) Sirtuin Functions in Health and Disease. Molecular Endocrinology, 21, 1745–1755. https://doi.org/10.1210/me.2007-0079 [3] Morris BJ (2013) Seven sirtuins for seven deadly diseases ofaging. Free Radical Biology and Medicine, 56, 133–171. https://doi.org/10.1016/j.freeradbiomed.2012.10.525 [4] Bordo D Structure and Evolution of Human Sirtuins. Current Drug Targets, 14, 662–665. http://dx.doi.org/10.2174/1389450111314060007 [5] Opazo JC, Vandewege MW, Hoffmann FG, Zavala K, Meléndez C, Luchsinger C, Cavieres VA, Vargas-Chacoff L, Morera FJ, Burgos PV, Tapia-Rojas C, Mardones GA (2022) How many sirtuin genes are out there? evolution of sirtuin genes in vertebrates with a description of a new family member. bioRxiv, 2020.07.17.209510, ver. 5 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2020.07.17.209510 [6] Eisen JA (1998) Phylogenomics: Improving Functional Predictions for Uncharacterized Genes by Evolutionary Analysis. Genome Research, 8, 163–167. https://doi.org/10.1101/gr.8.3.163 | How many sirtuin genes are out there? evolution of sirtuin genes in vertebrates with a description of a new family member | Juan C. Opazo, Michael W. Vandewege, Federico G. Hoffmann, Kattina Zavala, Catalina Meléndez, Charlotte Luchsinger, Viviana A. Cavieres, Luis Vargas-Chacoff, Francisco J. Morera, Patricia V. Burgos, Cheril Tapia-Rojas, Gonzalo A. Mardones | <p style="text-align: justify;">Studying the evolutionary history of gene families is a challenging and exciting task with a wide range of implications. In addition to exploring fundamental questions about the origin and evolution of genes, disent... | | Molecular Evolution | Frédéric Delsuc | Filipe Castro, Anonymous, Nicolas Leurs | 2022-05-12 16:06:04 | |
31 Mar 2022
Gene network robustness as a multivariate characterGenetic and environmental robustness are distinct yet correlated evolvable traits in a gene networkRecommended by Frédéric Guillaume based on reviews by Diogo Melo, Charles Mullon and Charles Rocabert
Organisms often show robustness to genetic or environmental perturbations. Whether these two components of robustness can evolve separately is the focus of the paper by Le Rouzic [1]. Using theoretical analysis and individual-based computer simulations of a gene regulatory network model, he shows that multiple aspects of robustness can be investigated as a set of pleiotropically linked quantitative traits. While genetically correlated, various robustness components (e.g., mutational, developmental, homeostasis) of gene expression in the regulatory network evolved more or less independently from each other under directional selection. The quantitative approach of Le Rouzic could explain both how unselected robustness components can respond to selection on other components and why various robustness-related features seem to have their own evolutionary history. Moreover, he shows that all components were evolvable, but not all to the same extent. Robustness to environmental disturbances and gene expression stability showed the largest responses while increased robustness to genetic disturbances was slower. Interestingly, all components were positively correlated and remained so after selection for increased or decreased robustness. This study is an important contribution to the discussion of the evolution of robustness in biological systems. While it has long been recognized that organisms possess the ability to buffer genetic and environmental perturbations to maintain homeostasis (e.g., canalization [2]), the genetic basis and evolutionary routes to robustness and canalization are still not well understood. Models of regulatory gene networks have often been used to address aspects of robustness evolution (e.g., [3]). Le Rouzic [1] used a gene regulatory network model derived from Wagner’s model [4]. The model has as end product the expression level of a set of genes influenced by a set of regulatory elements (e.g., transcription factors). The level and stability of expression are a property of the regulatory interactions in the network. Le Rouzic made an important contribution to the study of such gene regulation models by using a quantitative genetics approach to the evolution of robustness. He crafted a way to assess the mutational variability and selection response of the components of robustness he was interested in. Le Rouzic’s approach opens avenues to investigate further aspects of gene network evolutionary properties, for instance to understand the evolution of phenotypic plasticity. Le Rouzic also discusses ways to measure his different robustness components in empirical studies. As the model is about gene expression levels at a set of protein-coding genes influenced by a set of regulatory elements, it naturally points to the possibility of using RNA sequencing to measure the variation of gene expression in know gene networks and assess their robustness. Robustness could then be studied as a multidimensional quantitative trait in an experimental setting. References [1] Le Rouzic, A (2022) Gene network robustness as a multivariate character. arXiv: 2101.01564, ver. 5 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://arxiv.org/abs/2101.01564 [2] Waddington CH (1942) Canalization of Development and the Inheritance of Acquired Characters. Nature, 150, 563–565. https://doi.org/10.1038/150563a0 [3] Draghi J, Whitlock M (2015) Robustness to noise in gene expression evolves despite epistatic constraints in a model of gene networks. Evolution, 69, 2345–2358. https://doi.org/10.1111/evo.12732 [4] Wagner A (1994) Evolution of gene networks by gene duplications: a mathematical model and its implications on genome organization. Proceedings of the National Academy of Sciences, 91, 4387–4391. https://doi.org/10.1073/pnas.91.10.4387 | Gene network robustness as a multivariate character | Arnaud Le Rouzic | <p style="text-align: justify;">Robustness to genetic or environmental disturbances is often considered as a key property of living systems. Yet, in spite of being discussed since the 1950s, how robustness emerges from the complexity of genetic ar... | | Bioinformatics & Computational Biology, Evolutionary Theory, Genotype-Phenotype, Quantitative Genetics | Frédéric Guillaume | Charles Mullon, Charles Rocabert, Diogo Melo | 2021-01-11 17:48:20 | |
02 Feb 2023
Heterogeneities in infection outcomes across species: sex and tissue differences in virus susceptibilitySusceptibility to infection is not explained by sex or differences in tissue tropism across different species of DrosophilaRecommended by Alison Duncan based on reviews by Greg Hurst and 1 anonymous reviewerUnderstanding factors explaining both intra and interspecific variation in susceptibility to infection by parasites remains a key question in evolutionary biology. Within a species variation in susceptibility is often explained by differences in behaviour affecting exposure to infection and/or resistance affecting the degree by which parasite growth is controlled (Roy & Kirchner, 2000, Behringer et al., 2000). This can vary between the sexes (Kelly et al., 2018) and may be explained by the ability of a parasite to attack different organs or tissues (Brierley et al., 2019). However, what goes on within one species is not always relevant to another, making it unclear when patterns can be scaled up and generalised across species. This is also important to understand when parasites may jump hosts, or identify species that may be susceptible to a host jump (Longdon et al., 2015). Phylogenetic distance between hosts is often an important factor explaining susceptibility to a particular parasite in plant and animal hosts (Gilbert & Webb, 2007, Faria et al., 2013). In two separate experiments, Roberts and Longdon (Roberts & Longdon, 2022) investigated how sex and tissue tropism affected variation in the load of Drosophila C Virus (DCV) across multiple Drosophila species. DCV load has been shown to correlate positively with mortality (Longdon et al., 2015). Overall, they found that load did not vary between the sexes; within a species males and females had similar DCV loads for 31 different species. There was some variation in levels of DCV growth in different tissue types, but these too were consistent across males for 7 species of Drosophila. Instead, in both experiments, host phylogeny or interspecific variation, explained differences in DCV load with some species being more infected than others. This study is neat in that it incorporates and explores simultaneously both intra and interspecific variation in infection-related life-history traits which is not often done (but see (Longdon et al., 2015, Imrie et al., 2021, Longdon et al., 2011, Johnson et al., 2012). Indeed, most studies to date explore either inter-specific differences in susceptibility to a parasite (it can or can’t infect a given species) (Davies & Pedersen, 2008, Pfenning-Butterworth et al., 2021) or intra-specific variability in infection-related traits (infectivity, resistance etc.) due to factors such as sex, genotype and environment (Vale et al., 2008, Lambrechts et al., 2006). This work thus advances on previous studies, while at the same time showing that sex differences in parasite load are not necessarily pervasive. References Behringer DC, Butler MJ, Shields JD (2006) Avoidance of disease by social lobsters. Nature, 441, 421–421. https://doi.org/10.1038/441421a Brierley L, Pedersen AB, Woolhouse MEJ (2019) Tissue tropism and transmission ecology predict virulence of human RNA viruses. PLOS Biology, 17, e3000206. https://doi.org/10.1371/journal.pbio.3000206 Davies TJ, Pedersen AB (2008) Phylogeny and geography predict pathogen community similarity in wild primates and humans. Proceedings of the Royal Society B: Biological Sciences, 275, 1695–1701. https://doi.org/10.1098/rspb.2008.0284 Faria NR, Suchard MA, Rambaut A, Streicker DG, Lemey P (2013) Simultaneously reconstructing viral cross-species transmission history and identifying the underlying constraints. Philosophical Transactions of the Royal Society B: Biological Sciences, 368, 20120196. https://doi.org/10.1098/rstb.2012.0196 Gilbert GS, Webb CO (2007) Phylogenetic signal in plant pathogen–host range. Proceedings of the National Academy of Sciences, 104, 4979–4983. https://doi.org/10.1073/pnas.0607968104 Imrie RM, Roberts KE, Longdon B (2021) Between virus correlations in the outcome of infection across host species: Evidence of virus by host species interactions. Evolution Letters, 5, 472–483. https://doi.org/10.1002/evl3.247 Johnson PTJ, Rohr JR, Hoverman JT, Kellermanns E, Bowerman J, Lunde KB (2012) Living fast and dying of infection: host life history drives interspecific variation in infection and disease risk. Ecology Letters, 15, 235–242. https://doi.org/10.1111/j.1461-0248.2011.01730.x Kelly CD, Stoehr AM, Nunn C, Smyth KN, Prokop ZM (2018) Sexual dimorphism in immunity across animals: a meta-analysis. Ecology Letters, 21, 1885–1894. https://doi.org/10.1111/ele.13164 Lambrechts L, Chavatte J-M, Snounou G, Koella JC (2006) Environmental influence on the genetic basis of mosquito resistance to malaria parasites. Proceedings of the Royal Society B: Biological Sciences, 273, 1501–1506. https://doi.org/10.1098/rspb.2006.3483 Longdon B, Hadfield JD, Day JP, Smith SCL, McGonigle JE, Cogni R, Cao C, Jiggins FM (2015) The Causes and Consequences of Changes in Virulence following Pathogen Host Shifts. PLOS Pathogens, 11, e1004728. https://doi.org/10.1371/journal.ppat.1004728 Longdon B, Hadfield JD, Webster CL, Obbard DJ, Jiggins FM (2011) Host Phylogeny Determines Viral Persistence and Replication in Novel Hosts. PLOS Pathogens, 7, e1002260. https://doi.org/10.1371/journal.ppat.1002260 Pfenning-Butterworth AC, Davies TJ, Cressler CE (2021) Identifying co-phylogenetic hotspots for zoonotic disease. Philosophical Transactions of the Royal Society B: Biological Sciences, 376, 20200363. https://doi.org/10.1098/rstb.2020.0363 Roberts KE, Longdon B (2023) Heterogeneities in infection outcomes across species: examining sex and tissue differences in virus susceptibility. bioRxiv 2022.11.01.514663, ver. 2 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2022.11.01.514663 Roy BA, Kirchner JW (2000) Evolutionary Dynamics of Pathogen Resistance and Tolerance. Evolution, 54, 51–63. https://doi.org/10.1111/j.0014-3820.2000.tb00007.x Vale PF, Stjernman M, Little TJ (2008) Temperature-dependent costs of parasitism and maintenance of polymorphism under genotype-by-environment interactions. Journal of Evolutionary Biology, 21, 1418–1427. https://doi.org/10.1111/j.1420-9101.2008.01555.x | Heterogeneities in infection outcomes across species: sex and tissue differences in virus susceptibility | Katherine E Roberts, Ben Longdon | <p style="text-align: justify;">Species vary in their susceptibility to pathogens, and this can alter the ability of a pathogen to infect a novel host. However, many factors can generate heterogeneity in infection outcomes, obscuring our ability t... | | Evolutionary Ecology | Alison Duncan | Anonymous, Greg Hurst | 2022-11-03 11:17:42 | |
10 Jan 2019
Genomic data provides new insights on the demographic history and the extent of recent material transfers in Norway spruceDisentangling the recent and ancient demographic history of European spruce speciesRecommended by Jason Holliday based on reviews by 1 anonymous reviewerGenetic diversity in temperate and boreal forests tree species has been strongly affected by late Pleistocene climate oscillations [2,3,5], but also by anthropogenic forces. Particularly in Europe, where a long history of human intervention has re-distributed species and populations, it can be difficult to know if a given forest arose through natural regeneration and gene flow or through some combination of natural and human-mediated processes. This uncertainty can confound inferences of the causes and consequences of standing genetic variation, which may impact our interpretation of demographic events that shaped species before humans became dominant on the landscape. In their paper entitled "Genomic data provides new insights on the demographic history and the extent of recent material transfers in Norway spruce", Chen et al. [1] used a genome-wide dataset of 400k SNPs to infer the demographic history of Picea abies (Norway spruce), the most widespread and abundant spruce species in Europe, and to understand its evolutionary relationship with two other spruces (Picea obovata [Siberian spruce] and P. omorika [Serbian spruce]). Three major Norway spruce clusters were identified, corresponding to central Europe, Russia and the Baltics, and Scandinavia, which agrees with previous studies. The density of the SNP data in the present paper enabled inference of previously uncharacterized admixture between these groups, which corresponds to the timing of postglacial recolonization following the last glacial maximum (LGM). This suggests that multiple migration routes gave rise to the extant distribution of the species, and may explain why Chen et al.'s estimates of divergence times among these major Norway spruce groups were older (15mya) than those of previous studies (5-6mya) – those previous studies may have unknowingly included admixed material [4]. Treemix analysis also revealed extensive admixture between Norway and Siberian spruce over the last ~100k years, while the geographically-restricted Serbian spruce was both isolated from introgression and had a dramatically smaller effective population size (Ne) than either of the other two species. This small Ne resulted from a bottleneck associated with the onset of the iron age ~3000 years ago, which suggests that anthropogenic depletion of forest resources has severely impacted this species. Finally, ancestry of Norway spruce samples collected in Sweden and Denmark suggest their recent transfer from more southern areas of the species range. This northward movement of genotypes likely occurred because the trees performed well relative to local provenances, which is a common observation when trees from the south are planted in more northern locations (although at the potential cost of frost damage due to inappropriate phenology). While not the reason for the transfer, the incorporation of southern seed sources into the Swedish breeding and reforestation program may lead to more resilient forests under climate change. Taken together, the data and analysis presented in this paper allowed inference of the intra- and interspecific demographic histories of a tree species group at a very high resolution, and suggest caveats regarding sampling and interpretation of data from areas with a long history of occupancy by humans. References [1] Chen, J., Milesi, P., Jansson, G., Berlin, M., Karlsson, B., Aleksić, J. M., Vendramin, G. G., Lascoux, M. (2018). Genomic data provides new insights on the demographic history and the extent of recent material transfers in Norway spruce. BioRxiv, 402016. ver. 3 peer-reviewed and recommended by PCI Evol Biol. doi: 10.1101/402016 | Genomic data provides new insights on the demographic history and the extent of recent material transfers in Norway spruce | Jun Chen, Lili Li, Pascal Milesi, Gunnar Jansson, Mats Berlin, Bo Karlsson, Jelena Aleksic, Giovanni G Vendramin, Martin Lascoux | <p>Primeval forests are today exceedingly rare in Europe and transfer of forest reproductive material for afforestation and improvement have been very common, especially over the last two centuries. This can be a serious impediment when inferring ... | | Evolutionary Applications, Hybridization / Introgression, Population Genetics / Genomics | Jason Holliday | Anonymous, Anonymous | 2018-08-29 08:33:15 | |
08 Aug 2018
Sexual selection and inbreeding: two efficient ways to limit the accumulation of deleterious mutationsInbreeding compensates for reduced sexual selection in purging deleterious mutationsRecommended by Charles Baer based on reviews by 2 anonymous reviewersTwo evolutionary processes have been shown in theory to enhance the effects of natural selection in purging deleterious mutations from a population (here ""natural"" selection is defined as ""selection other than sexual selection""). First, inbreeding, especially self-fertilization, facilitates the removal of deleterious recessive alleles, the effects of which are largely hidden from selection in heterozygotes when mating is random. Second, sexual selection can facilitate the removal of deleterious alleles of arbitrary dominance, with little or no demographic cost, provided that deleterious effects are greater in males than in females (""genic capture""). Inbreeding (especially selfing) and sexual selection are often negatively correlated in nature. Empirical tests of the role of sexual selection in purging deleterious mutations have been inconsistent, potentially due to the positive relationship between sexual selection and intersexual genetic conflict. References [1] Noël, E., Fruitet, E., Lelaurin, D., Bonel, N., Segard, A., Sarda, V., Jarne, P., & David P. (2018). Sexual selection and inbreeding: two efficient ways to limit the accumulation of deleterious mutations. bioRxiv, 273367, ver. 3 recommended and peer-reviewed by PCI Evol Biol. doi: 10.1101/273367 | Sexual selection and inbreeding: two efficient ways to limit the accumulation of deleterious mutations | E. Noël, E. Fruitet, D. Lelaurin, N. Bonel, A. Ségard, V. Sarda, P. Jarne and P. David | <p>This preprint has been reviewed and recommended by Peer Community In Evolutionary Biology (https://dx.doi.org/10.24072/pci.evolbiol.100055). Theory and empirical data showed that two processes can boost selection against deleterious mutations, ... | | Adaptation, Experimental Evolution, Reproduction and Sex, Sexual Selection | Charles Baer | Anonymous | 2018-03-01 08:12:37 | |
12 Nov 2020
Limits and Convergence properties of the Sequentially Markovian CoalescentReview and Assessment of Performance of Genomic Inference Methods based on the Sequentially Markovian CoalescentRecommended by Stephan Schiffels based on reviews by 3 anonymous reviewers
The 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 | |
25 Sep 2023
Random genetic drift sets an upper limit on mRNA splicing accuracy in metazoansThe drift barrier hypothesis and the limits to alternative splicing accuracyRecommended by Ignacio Bravo based on reviews by Lars M. Jakt and 2 anonymous reviewersAccurate information flow is central to living systems. The continuity of genomes through generations as well as the reproducible functioning and survival of the individual organisms require a faithful information transfer during replication, transcription and translation. The differential efficiency of natural selection against “mistakes” results in decreasing fidelity rates for replication, transcription and translation. At each level in the information flow chain (replication, transcription, translation), numerous complex molecular systems have evolved and been selected for preventing, identifying and, when possible, correcting or removing such “mistakes” arising during information transfer. However, fidelity cannot be improved ad infinitum. First, because of the limits imposed by the physical nature of the processes of copying and recoding information over different molecular supports: all mechanisms ensuring fidelity during biological information transfer ultimately rely on chemical kinetics and thermodynamics. The more accurate a copying process is, the lower the synthesis rate and the higher the energetic cost of correcting errors. Second, because of the limits imposed by random genetic drift: natural selection cannot effectively act on an allele that contributes with a small differential advantage unless effective population size is large. If s <1/Ne (or s <1/(2Ne) in diploids) the allele frequency in the population is de facto subject to neutral drift processes. In their preprint “Random genetic drift sets an upper limit on mRNA splicing accuracy in metazoans”, Bénitière, Necsulea and Duret explore the validity of this last mentioned “drift barrier” hypothesis for the case study of alternative splicing diversity in eukaryotes (Bénitière et al. 2022). Splicing refers to an ensemble of eukaryotic molecular processes mediated by a large number of proteins and ribonucleoproteins and involving nucleotide sequence recognition, that uses as a molecular substrate a precursor messenger RNA (mRNA), directly transcribed from the DNA, and produces a mature mRNA by removing introns and joining exons (Chow et al. 1977). Alternative splicing refers to the case in which different molecular species of mature mRNAs can be produced, either by cis-splicing processes acting on the same precursor mRNA, e.g. by varying the presence/absence of different exons or by varying the exon-exon boundaries, or by trans-splicing processes, joining exons from different precursor mRNA molecules. The diversity of mRNA molecular species generated by alternative splicing enlarges the molecular phenotypic space that can be generated from the same genotype. In humans, alternative splicing occurs in around 95% of the ca. 20,000 genes, resulting in ca. 100,000 medium-to-high abundance transcripts (Pan et al. 2008). In multicellular organisms, the frequency of alternatively spliced mRNAs varies between tissues and across ontogeny, often in a switch-like pattern (Wang et al. 2008). In the molecular and cell biology community, it is commonly accepted that splice variants contribute with specific functions (Marasco and Kornblihtt 2023) although there exists a discussion around the functional nature of low-frequency splice variants (see for instance the debate between Tress et al. 2017 and Blencowe 2017). The origin, diversity, regulation and evolutionary advantage of alternative splicing constitutes thus a playground of the selectionist-neutralist debate, with one extreme considering that most splice variants are mere “mistakes” of the splicing process (Pickrell et al. 2010), and the other extreme considering that alternative splicing is at the core of complexity in multicellular organisms, as it increases the genome coding potential and allows for a large repertoire of cell types (Chen et al. 2014). In their manuscript, Bénitière, Necsulea and Duret set the cursor towards the neutralist end of the gradient and test the hypothesis of whether the high alternative splice rate in “complex” organisms corresponds to a high rate of splicing “mistakes”, arising from the limit imposed by the drift barrier effect on the power of natural selection to increase accuracy (Bush et al. 2017). In their preprint, the authors convincingly show that in metazoans a fraction of the variation of alternative splicing rate is explained by variation in proxies of population size, so that species with smaller Ne display higher alternative splice rates. They communicate further that abundant splice variants tend to preserve the reading frame more often than low-frequency splice variants, and that the nucleotide splice signals in abundant splice variants display stronger evidence of purifying selection than those in low-frequency splice variants. From all the evidence presented in the manuscript, the authors interpret that “variation in alternative splicing rate is entirely driven by variation in the efficacy of selection against splicing errors”. The authors honestly present some of the limitations of the data used for the analyses, regarding i) the quality of the proxies used for Ne (i.e. body length, longevity and dN/dS ratio); ii) the heterogeneous nature of the RNA sequencing datasets (full organisms, organs or tissues; different life stages, sexes or conditions); and iii) mostly short RNA reads that do not fully span individual introns. Further, data from bacteria do not verify the herein communicated trends, as it has been shown that bacterial species with low population sizes do not display higher transcription error rates (Traverse and Ochman 2016). Finally, it will be extremely interesting to introduce a larger evolutionary perspective on alternative splicing rates encompassing unicellular eukaryotes, in which an intriguing interplay between alternative splicing and gene duplication has been communicated (Hurtig et al. 2020). The manuscript from Bénitière, Necsulea and Duret makes a significant advance to our understanding of the diversity, the origin and the physiology of post-transcriptional and post-translational mechanisms by emphasising the fundamental role of non-adaptive evolutionary processes and the upper limits to splicing accuracy set by genetic drift. References Bénitière F, Necsulea A, Duret L. 2023. Random genetic drift sets an upper limit on mRNA splicing accuracy in metazoans. bioRxiv, ver. 4 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2022.12.09.519597 Blencowe BJ. 2017. The Relationship between Alternative Splicing and Proteomic Complexity. Trends Biochem Sci 42:407–408. https://doi.org/10.1016/j.tibs.2017.04.001 Bush SJ, Chen L, Tovar-Corona JM, Urrutia AO. 2017. Alternative splicing and the evolution of phenotypic novelty. Philos Trans R Soc Lond B Biol Sci 372:20150474. https://doi.org/10.1098/rstb.2015.0474 Chen L, Bush SJ, Tovar-Corona JM, Castillo-Morales A, Urrutia AO. 2014. Correcting for differential transcript coverage reveals a strong relationship between alternative splicing and organism complexity. Mol Biol Evol 31:1402–1413. https://doi.org/10.1093/molbev/msu083 Chow LT, Gelinas RE, Broker TR, Roberts RJ. 1977. An amazing sequence arrangement at the 5’ ends of adenovirus 2 messenger RNA. Cell 12:1–8. https://doi.org/10.1016/0092-8674(77)90180-5 Hurtig JE, Kim M, Orlando-Coronel LJ, Ewan J, Foreman M, Notice L-A, Steiger MA, van Hoof A. 2020. Origin, conservation, and loss of alternative splicing events that diversify the proteome in Saccharomycotina budding yeasts. RNA 26:1464–1480. https://doi.org/10.1261/rna.075655.120 Marasco LE, Kornblihtt AR. 2023. The physiology of alternative splicing. Nat Rev Mol Cell Biol 24:242–254. https://doi.org/10.1038/s41580-022-00545-z Pan Q, Shai O, Lee LJ, Frey BJ, Blencowe BJ. 2008. Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing. Nat Genet 40:1413–1415. https://doi.org/10.1038/ng.259 Pickrell JK, Pai AA, Gilad Y, Pritchard JK. 2010. Noisy splicing drives mRNA isoform diversity in human cells. PLoS Genet 6:e1001236. https://doi.org/10.1371/journal.pgen.1001236 Traverse CC, Ochman H. 2016. Conserved rates and patterns of transcription errors across bacterial growth states and lifestyles. Proc Natl Acad Sci U S A 113:3311–3316. https://doi.org/10.1073/pnas.1525329113 Tress ML, Abascal F, Valencia A. 2017. Alternative Splicing May Not Be the Key to Proteome Complexity. Trends Biochem Sci 42:98–110. https://doi.org/10.1016/j.tibs.2016.08.008 Wang ET, Sandberg R, Luo S, Khrebtukova I, Zhang L, Mayr C, Kingsmore SF, Schroth GP, Burge CB. 2008. Alternative isoform regulation in human tissue transcriptomes. Nature 456:470–476. https://doi.org/10.1038/nature07509 | Random genetic drift sets an upper limit on mRNA splicing accuracy in metazoans | Florian Benitiere, Anamaria Necsulea, Laurent Duret | <p style="text-align: justify;">Most eukaryotic genes undergo alternative splicing (AS), but the overall functional significance of this process remains a controversial issue. It has been noticed that the complexity of organisms (assayed by the nu... | | Bioinformatics & Computational Biology, Genome Evolution, Molecular Evolution, Population Genetics / Genomics | Ignacio Bravo | Anonymous | 2022-12-12 14:00:01 | |
21 Feb 2023
Wolbachia genomics reveals a potential for a nutrition-based symbiosis in blood-sucking Triatomine bugsNutritional symbioses in triatomines: who is playing?Recommended by Natacha Kremer based on reviews by Alejandro Manzano Marín and Olivier DuronNearly 8 million people are suffering from Chagas disease in the Americas. The etiological agent, Trypanosoma cruzi, is mainly transmitted by triatomine bugs, also known as kissing or vampire bugs, which suck blood and transmit the parasite through their feces. Among these triatomine species, Rhodnius prolixus is considered the main vector, and many studies have focused on characterizing its biology, physiology, ecology and evolution. Interestingly, given that Rhodnius species feed almost exclusively on blood, their diet is unbalanced, and the insects can lack nutrients and vitamins that they cannot synthetize themself, such as B-vitamins. In all insects feeding exclusively on blood, symbioses with microbes producing B-vitamins (mainly biotin, riboflavin and folate) have been widely described (see review in Duron and Gottlieb 2020) and are critical for insect development and reproduction. These co-evolved relationships between blood feeders and nutritional symbionts could now be considered to develop new control methods, by targeting the ‘Achille’s heel’ of the symbiotic association (i.e., transfer of nutrient and / or control of nutritional symbiont density). But for this, it is necessary to better characterize the relationships between triatomines and their symbionts. R. prolixus is known to be associated with several symbionts. The extracellular gut symbiont Rhodococcus rhodnii, which reaches high bacterial densities and is almost fixed in R. prolixus populations, appears to be a nutritional symbiont under many blood sources. This symbiont can provide B-vitamins such as biotin (B7), niacin (B3), thiamin (B1), pyridoxin (B6) or riboflavin (B2) and can play an important role in the development and the reproduction of R. prolixus (Pachebat et al. (2013) and see review in Salcedo-Porras et al. (2020)). This symbiont is orally acquired through egg smearing, ensuring the fidelity of transmission of the symbiont from mother to offspring. However, as recently highlighted by Tobias et al. (2020) and Gilliland et al. (2022), other gut microbes could also participate to the provision of B-vitamins, and R. rhodnii could additionally provide metabolites (other than B-vitamins) increasing bug fitness. In the study from Filée et al., the authors focused on Wolbachia, an intracellular, maternally inherited bacterium, known to be a nutritional symbiont in other blood-sucking insects such as bedbugs (Nikoh et al. 2014), and its potential role in vitamin provision in triatomine bugs. After screening 17 different triatomine species from the 3 phylogenetic groups prolixus, pallescens and pictipes, they first show that Wolbachia symbionts are widely distributed in the different Rhodnius species. Contrary to R. rhodnii that were detected in all samples, Wolbachia prevalence was patchy and rarely fixed. The authors then sequenced, assembled, and compared 13 Wolbachia genomes from the infected Rhodnius species. They showed that all Wolbachia are phylogenetically positioned in the supergroup F that contains wCle (the Wolbachia from bedbugs). In addition, 8 Wolbachia strains (out of 12) encode a biotin operon under strong purifying selection, suggesting the preservation of the biological function and the metabolic potential of Wolbachia to supplement biotin in their Rhodnius host. From the study of insect genomes, the authors also evidenced several horizontal transfers of genes from Wolbachia to Rhodnius genomes, which suggests a complex evolutionary interplay between vampire bugs and their intracellular symbiont. This nice piece of work thus provides valuable information to the fields of multiple partners / nutritional symbioses and Wolbachia research. Dual symbioses described in insects feeding on unbalanced diets generally highlight a certain complementarity between symbionts that ensure the whole nutritional complementation. The study presented by Filée et al. leads rather to consider the impact of multiple symbionts with different lifestyles and transmission modes in the provision of a specific nutritional benefit (here, biotin). Because of the low prevalence of Wolbachia in certain species, a “ménage à trois” scenario would rather be replaced by an “open couple”, where the host relationship with new symbiotic partners (more or less stable at the evolutionary timescale) could provide benefits in certain ecological situations. The results also support the potential for Wolbachia to evolve rapidly along a continuum between parasitism and mutualism, by acquiring operons encoding critical pathways of vitamin biosynthesis. References Duron O. and Gottlieb Y. (2020) Convergence of Nutritional Symbioses in Obligate Blood Feeders. Trends in Parasitology 36(10):816-825. https://doi.org/10.1016/j.pt.2020.07.007 Filée J., Agésilas-Lequeux K., Lacquehay L., Bérenger J.-M., Dupont L., Mendonça V., Aristeu da Rosa J. and Harry M. (2023) Wolbachia genomics reveals a potential for a nutrition-based symbiosis in blood-sucking Triatomine bugs. bioRxiv, 2022.09.06.506778, ver. 3 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2022.09.06.506778 Gilliland C.A. et al. (2022) Using axenic and gnotobiotic insects to examine the role of different microbes on the development and reproduction of the kissing bug Rhodnius prolixus (Hemiptera: Reduviidae). Molecular Ecology. https://doi.org/10.1111/mec.16800 Nikoh et al. (2014) Evolutionary origin of insect–Wolbachia nutritional mutualism. PNAS. 111(28):10257-10262. https://doi.org/10.1073/pnas.1409284111 Pachebat, J.A. et al. (2013). Draft genome sequence of Rhodococcus rhodnii strain LMG5362, a symbiont of Rhodnius prolixus (Hemiptera, Reduviidae, Triatominae), the principle vector of Trypanosoma cruzi. Genome Announc. 1(3):e00329-13. https://doi.org/10.1128/genomea.00329-13 Salcedo-Porras N., et al. (2020). The role of bacterial symbionts in Triatomines: an evolutionary perspective. Microorganisms. 8:1438. https://doi.org/10.3390%2Fmicroorganisms8091438 Tobias N.J., Eberhard F.E., Guarneri A.A. (2020) Enzymatic biosynthesis of B-complex vitamins is supplied by diverse microbiota in the Rhodnius prolixus anterior midgut following Trypanosoma cruzi infection. Computational and Structural Biotechnology Journal. 3395-3401. https://doi.org/10.1016/j.csbj.2020.10.031 | Wolbachia genomics reveals a potential for a nutrition-based symbiosis in blood-sucking Triatomine bugs | Jonathan Filée, Kenny Agésilas-Lequeux, Laurie Lacquehay, Jean Michel Bérenger, Lise Dupont, Vagner Mendonça, João Aristeu da Rosa, Myriam Harry | <p>The nutritional symbiosis promoted by bacteria is a key determinant for adaptation and evolution of many insect lineages. A complex form of nutritional mutualism that arose in blood-sucking insects critically depends on diverse bacterial symbio... | | Genome Evolution, Phylogenetics / Phylogenomics, Species interactions | Natacha Kremer | Alejandro Manzano Marín | 2022-09-13 17:36:46 |
