Biology subjects

Lenormand, T.

Publications and source records attributed to Lenormand, T..

15 recordsLinked to original sources

bioRxiv2026

Inferring the multi-host fitness landscape of endive necrotic mosaic virus from cross-inoculation experiments

Fitness landscapes offer a compact representation of adaptation, yet are rarely inferred from sparse multi-environment data. We present a Bayesian approach to infer an effective multi-host phenotypic fitness landscape from cross-inoculation assays by linking successful infection probabilities to Fishers geometrical model and to an explicit decomposition of establishment routes. The model estimates (i) the distance matrix among host-specific phenotypic optima, (ii) target-host permissiveness through the widths of fitness peaks, (iii) target-specific differences in the efficiency with which phenotypic suitability translates into successful infection, and (iv) the conditional probabilities that successful infections are attributed to direct establishment, rescue from standing variation in the source inoculum, or de novo rescue in the target host. We apply the approach to an experimental evolution dataset for endive necrotic mosaic virus evolved on five Asteraceae hosts and challenged in a full cross-inoculation design. The inferred landscape can be visualized as a phenotypic map of the host community, revealing pronounced heterogeneity in target-host permissiveness and a geometry broadly concordant with host phylogeny. By grounding assay-derived distances in an explicit mechanistic model, the approach provides a parsimonious representation of multi-host constraints that can be used to discuss establishment barriers and potential springboard hosts in heterogeneous communities. More broadly, it offers a general method for inferring effective fitness landscapes from sparse multi-environment data.

evolutionary biology↗

bioRxiv2025

Effects of deleterious mutations on the fixation of chromosomal inversions on autosomes and sex chromosomes

Deleterious mutations have multiple effects on the fate of chromosomal inversions. In this article, we use individual-based simulations to estimate the fixation probabilities of neutral inversions under a constant input of deleterious mutations. As shown previously, we find that lucky inversions carrying a lower-than-average mutation load are initially favored and tend to selectively spread. Our results also outline the importance of Mullers ratchet caused by the absence of recombination in Y-linked and in rare autosomal inversions, reducing their fixation probabilities. Despite the fact that Y-linked inversions are more susceptible to Mullers ratchet, they can more easily fix than autosomal inversions despite initially carrying mutations, when these mutations have sufficiently low selection or dominance coefficients (sheltering effect). Similarly, the sheltering of deleterious alleles can increase the fixation probability of inversions capturing a mating-type locus, particularly under intermediate rates of self-fertilization. Overall, our results confirm that when mating is random and for realistic parameter values, the presence of deleterious alleles reduces the average fixation probability of autosomal, sex-linked or mating type-linked inversions below that of a neutral mutation. Nevertheless, the occasional fixation of a lucky inversion may have important macroevolutionary consequences, potentially contributing to the evolution of recombination arrest on sex chromosomes.

evolutionary biology↗

bioRxiv2024

A single theory for the evolution of sex chromosomes and the two rules of speciation

Sex chromosomes are involved in three major empirical patterns: Y (or W) chromosomes are often non-recombining and degenerate; heterogametic offspring (XY or ZW) from interspecific crosses are more often sterile or inviable than homogametic offspring (Haldanes rule); the X (or Z) has a disproportionately large effect on reproductive isolation between species compared to autosomes (the large X effect). Each observation has received its own tailored explanation involving multiple genetic and evolutionary causes. Here, we show that these empirical patterns all emerge from a single theory for sex chromosome evolution incorporating the co-evolution of cis and trans-acting regulators of gene expression, and leading to systematic misexpression of dosage-compensated genes in heterogametic F1 hybrids, for both young and old sex chromosomes. Structured AbstractO_ST_ABSIntroductionC_ST_ABSSex chromosomes have long been known to play a prominent role in the genetics of speciation, captured by the famous "two rules of speciation". The first, attributed to J.B.S. Haldane and known as Haldanes rule, corresponds to the general observation that when, among interspecific hybrids, one sex is inviable or sterile, it is more often the heterogametic sex (XY or ZW). The second is known as the large X effect, and refers to the fact that the X or Z chromosome often has a stronger effect on hybrid fitness than autosomes of equivalent size. While several theories have been proposed to explain these empirical patterns, none has been able to account for all the observations, leading to the current consensus that the two rules of speciation may have multiple causes. Furthermore, these theories remain disconnected from general models predicting sex chromosome evolution. RationaleWe have recently developed a new theory for the evolution of sex chromosomes, showing that the coevolution of cis and trans regulators of gene expression can lead to stable recombination arrest between the X and Y (or Z and W) chromosomes, degeneration of the Y (or W) chromosome and dosage compensation. Here we investigate the role of sex chromosomes on the fitness of interspecific hybrids under this general model, considering different scenarios that correspond to different stages in the evolution of sex chromosomes. We also investigate the effect of genes with sex-specific effects that affect either male or female fertility. ResultsHaldanes rule and the large X effect are observed in all scenarios considered. Our model also captures "Darwins corollary" to Haldanes rule, i.e. an asymmetry between the effects of reciprocal crosses between species. These results are caused by the divergence of regulators of gene expression between species, due to the presence of a non-recombining, degenerate stratum on the Y chromosome either shared by both species or present in only one of them. In both cases, Haldanes rule results from the heterogametic sex inheriting X chromosome cis regulators from only one parental species that have not coevolved with the trans regulators of the other species, resulting in under or overexpression of dosage-compensated genes on the X (or Z) chromosome. While this regulatory divergence may be limited in the case of species with a global (chromosome-wide) somatic system of dosage compensation, regulatory divergence of germline-expressed genes may generate Haldanes rule for fertility in these species. Genes whose effect is restricted to the heterogametic sex often have strong effects on reproductive isolation and on the fitness of heterogametic hybrids, especially if they are silenced on the X (or Z) chromosome of one parental species and on the Y (or W) chromosome of the other. ConclusionOur study shows that a simple model of coevolution between cis and trans regulators of gene expression on sex chromosomes can explain the evolution of non-recombining, degenerate and dosage compensated Y and W chromosomes, Haldanes rule and the large X effect. It may also explain why Haldanes rule is based on viability is some taxa and on fertility in others, an observation that remained difficult to explain from previous theories. These results match with recent observations on the role of misregulation of gene expression on hybrid fitness, and open new perspectives of empirical research on the genetics of speciation. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=184 SRC="FIGDIR/small/585601v4_figa1.gif" ALT="Figure 1"> View larger version (45K): org.highwire.dtl.DTLVardef@e94472org.highwire.dtl.DTLVardef@8cbecaorg.highwire.dtl.DTLVardef@41cc5dorg.highwire.dtl.DTLVardef@1d00ea0_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOSummary figure.C_FLOATNO A multilocus, individual-based simulation model was used to investigate the joint evolution of sex chromosomes and reproductive isolation between species. It includes deleterious mutations, mutations suppressing or restoring recombination and mutations affecting the strength of cis and trans regulators of gene expression. This model predicts the major features of sex chromosome evolution and the "two rules of speciation" (Haldanes rule and the large X effect). C_FIG

evolutionary biology↗

bioRxiv2024

Transgenerational chromosome repair in the asexual bdelloid rotifer Adineta vaga

Homologous recombination is an essential DNA repair mechanism that promotes chromosome pairing and ensures allele segregation during meiosis in sexual organisms. Here, we explore the dual function of homologous recombination in the bdelloid rotifer Adineta vaga, an ancient asexual species known for its remarkable resilience to extreme genotoxic stresses. Genomic analyses reveal that A. vaga uses meiotic recombination, both to promote spontaneous crossovers and gene conversion during oogenesis and to repair the genome in response to DNA damage. Our study identifies a novel transgenerational DNA repair mechanism, termed break-induced homologous extension repair (BIHER), which operates on single DNA ends to repair fragmented chromosomes over successive generations. Our findings suggest that meiotic BIHER, coupled with the holocentric structure of chromosomes, represents a key adaptation of life in extreme environments.

evolutionary biology↗

bioRxiv2023

Revisiting the shelter theory: can deleterious mutations alone explain the evolution of sex chromosomes?

Y and W chromosomes often stop recombining and degenerate. Most work on recombination suppression has focused on the mechanisms favoring recombination arrest in the short term. Yet, the long-term maintenance of recombination suppression is critical to evolving degenerate sex chromosomes. This long-term maintenance has been little investigated. In the long term, recombination suppression may be maintained for selective reasons (e.g., involving the emergence of nascent dosage compensation), or due to mechanistic constraints preventing the reestablishment of recombination, for instance when complex chromosomal rearrangements evolve on the Y. In this paper, we investigate these constraint theories. We show that they face a series of theoretical difficulties: they are not robust to extremely low rates of recombination restoration; they would rather cause population extinction than Y degeneration; they are less efficient at producing a non-recombining and degenerate Y than scenarios adding a selective pressure against recombination, whatever the rate of recombination restoration. Finally, whether such very high constraints exist is questionable. Very low rates of recombination reestablishment are sufficient to prevent Y degeneration, given the large fitness advantage to recover a non-degenerate Y or W for the heterogametic sex. The assumption of a lack of genetic variation to restore recombination seems also implausible given known mechanisms to restore a recombining pair of sex chromosomes.

evolutionary biology↗

bioRxiv2022

The genetic architecture of local adaptation in a cline

Local adaptation is pervasive. It occurs whenever selection favors different phenotypes in different environments, provided that there is genetic variation for the corresponding traits and that the effect of selection is greater than the effect of drift and migration. In many cases, ecologically relevant traits are quantitative and controlled by many genes. It has been repeatedly proposed that the localization of these genes in the genome may not be random, but could be an evolved feature. In particular, the clustering of local adaptation genes may be theoretically expected and has been observed in several situations. Previous theory has focused on two-patch or continent-island models to investigate this phenomenon, reaching the conclusion that such clustering could evolve, but in relatively limited conditions. In particular, it required that migration rate was neither too low nor too large and that the full optimization of trait values could not be eventually achieved by a mutation at a single locus. Here, we investigate this question in a spatially-explicit model, considering two contiguous habitats with distinct trait optima on a circular stepping-stone. We find that clustering of local-adaptation genes is pervasive within clines during both the establishment phase of local adaptation and the subsequent "reconfiguration" phase where different genetic architectures compete with each other. We also show that changing the fitness function relating trait to fitness has a strong impact on the overall evolutionary dynamics and resulting architecture.

evolutionary biology↗

bioRxiv2022

Asexual male production by ZW recombination in Artemia parthenogenetica

In some asexual species, parthenogenetic females occasionally produce males, which may strongly affect the evolution and maintenance of asexuality if they cross with related sexuals and transmit genes causing asexuality to their offspring ("contagious parthenogenesis"). How these males arise in the first place has remained enigmatic, especially in species with sex chromosomes. Here, we test the hypothesis that rare, asexually produced males of the crustacean Artemia parthenogenetica are produced by recombination between the Z and W sex chromosomes during non-clonal parthenogenesis, resulting in ZZ males through loss of heterozygosity at the sex determination locus. We used RAD-sequencing to compare asexual mothers with their male and female offspring. Markers on several sex-chromosome scaffolds indeed lost heterozygosity in all male but no female offspring, suggesting that they correspond to the sex-determining region. Other sex-chromosome scaffolds lost heterozygosity in only a part of the male offspring, consistent with recombination occurring at a variable location. Alternative hypotheses for the production of these males (such as partial or total hemizygosity of the Z) could be excluded. Rare males are thus produced because recombination is not entirely suppressed during parthenogenesis in A. parthenogenetica. This finding may contribute to explaining the maintenance of recombination in these asexuals.

evolutionary biology↗

bioRxiv2021

No support for a meiosis suppressor in Daphnia pulex: Comparison of linkage maps reveals normal recombination in males of obligate parthenogenetic lineages.

It is often assumed that obligate parthenogenesis (OP) evolves by a disruption of meiosis and recombination. One emblematic example that appears to support this view is the crustacean Daphnia pulex. Here, by constructing high-density linkage maps, we estimate genome-wide recombination rates in males that are occasionally produced by OP lineages, as well as in males and females of cyclical parthenogenetic (CP) lineages. The results show no significant differences in recombination rates and patterns between CP and OP males nor between CP male and CP females. The observation that recombination is not suppressed in OP males invalidates the hypothesis of a general meiosis suppressor responsible for OP. Rather, our findings suggest that in D. pulex, as in other species where OP evolves from CP ancestors, the CP to OP transition evolves through a re-use of the parthenogenesis pathways already present in CP and through their extension to the entire life cycle, at least in females. In addition to the implications for the evolution of OP, the genetic maps produced by this study constitute an important genomic resource for the model species Daphnia.

evolutionary biology↗

bioRxiv2021

The origin of asexual brine shrimps

Determining how and how often asexual lineages emerge within sexual species is central to our understanding of sex-asex transitions and the long-term maintenance of sex. Asexuality can arise "by transmission" from an existing asexual lineage to a new one, through different types of crosses. The occurrence of these crosses, cryptic sex, variation in ploidy and recombination within asexuals greatly complicates the study of sex-asex transitions, as they preclude the use of standard phylogenetic methods and genetic distance metrics. In this study we show how to overcome these challenges by developing new approaches to investigate the origin of the various asexual lineages of the brine shrimp Artemia parthenogenetica. We use a large sample of asexuals, including all known polyploids, and their sexual relatives. We combine flow cytometry with mitochondrial and nuclear DNA data. We develop new genetic distance measures and methods to compare various scenarios describing the origin of the different lineages. We find that all diploid and polyploid A. parthenogenetica likely arose within the last 80,000 years through successive and nested hybridization events that involved backcrosses with different sexual species. All A. parthenogenetica have the same common ancestor and therefore likely carry the same asexuality gene(s) and reproduce by automixis. These findings radically change our view of sex-asex transitions in this group, and show the importance of considering asexuality "by transmission" scenarios. The methods developed are applicable to many other asexual taxa.

evolutionary biology↗

bioRxiv2021

Y recombination arrest and degeneration in the absence of sexual dimorphism

Current theory proposes degenerated sex chromosomes evolve via three successive steps: recombination arrest, which links male-beneficial alleles to the Y chromosome; degeneration of these regions due to the inefficacy of natural selection in the absence of recombination; and lastly, the evolution of dosage compensation to correct the resulting low expression of X-linked genes in males. Here we investigate new models of sex chromosome evolution incorporating the coevolution of cis- and trans-regulators of gene expression. We show that the early emergence of dosage compensation favors the maintenance of Y-linked inversions by creating sex-antagonistic regulatory effects. This is followed by inversion degeneration caused by regulatory divergence between the X and Y chromosomes. In stark contrast to the current theory, the whole process occurs without any selective pressure related to sexual dimorphism. One Sentence SummaryTurning sex chromosome theory on its head: early evolution of dosage compensation can maintain successively forming Y chromosome strata that undergo genetic degeneration.

evolutionary biology↗

bioRxiv2021

Strong transgenerational effects but no genetic adaptation in zooplankton 24 years after an abrupt +10°C climate change

The climate is currently warming fast, threatening biodiversity all over the globe. Adaptation is often rapid when the environment changes quickly, but for climate warming very little evidence is available. Here, we investigate the pattern of adaptation to an extreme +10{degrees}C climate change in the wild, following the introduction of brine shrimp Artemia franciscana from San Francisco Bay, USA, to Vinh Chau saltern in Vietnam. We use a resurrection ecology approach, hatching diapause eggs from the ancestral population and the introduced population after 13 and 24 years (resp. ~54 and ~100 generations). In a series of coordinated experiments, we determined whether the introduced Artemia show increased tolerance to higher temperatures, and the extent to which genetic adaptation, developmental plasticity, transgenerational effects, and local microbiome differences contributed to this tolerance. We find that introduced brine shrimp do show increased phenotypic tolerance to warming. Yet strikingly, these changes do not have an additive genetic component, are not caused by mitochondrial genetic variation, and are not caused by epigenetic marks set by adult parents exposed to warming. Further, we do not find any developmental plasticity in response to warming, nor any protective effect of heat-tolerant local microbiota. We conclude that the evolution of shrimps extreme thermal tolerance is only due to transgenerational (great)grandparental effects, possibly epigenetic marks set by parents who were exposed to high temperatures as juveniles. This finding challenges standard models of genetic and plastic adaptive responses, and our conception of how species may cope with climate warming. Significance statementAdaptation is often rapid when environments change quickly, but for climate warming little evidence is available. Many studies report no genetic responses due to pre-existing plasticity, while others point towards epigenetics and microbiota effects. In this study, we take advantage of a natural experiment to study all of these effects. We use a set of coordinated experiments and a resurrection ecology approach, reviving resting eggs of brine shrimp up to100 generations after their introduction from a temperate to a tropical saltern. We find that heat adaptation occurs, but heritability is fully "missing". Plasticity and microbiota play no role either, indicating that only transgenerational (great)grandmaternal effects are involved. This finding prompts us to reconsider the relative importance of the different possible mechanisms by which phenotypic change can occur, especially in response to temperature variation.

evolutionary biology↗

bioRxiv2019

Trait-specific trade-offs prevent niche expansion in two parasites

The evolution of host specialization has been studied intensively, yet it is still often difficult to determine why parasites do not evolve broader niches - in particular when the available hosts are closely related and ecologically similar. Here, we used an experimental evolution approach to study the evolution of host specialization, and its underlying traits, in two sympatric parasites: Anostracospora rigaudi and Enterocytospora artemiae, microsporidians infecting the brine shrimp Artemia franciscana and Artemia parthenogenetica. In the field, both parasites regularly infect both hosts, yet experimental work has revealed that they are each partially specialized. We serially passaged the parasites on one, the other, or an alternation of the two hosts; after ten passages, we assayed the infectivity, virulence, and spore production rate of the evolved lines. In accordance with previous studies, A. rigaudi maintained a higher fitness on A. parthenogenetica, and E. artemiae on A. franciscana, in all treatments. The origin of this specialization was not infectivity, which readily evolved and traded off weakly between the host species for both parasites. Instead, the overall specialization was caused by spore production, which did not evolve in any treatment. This suggests the existence of a strong trade-off between spore production in A. franciscana and spore production in A. parthenogenetica, making this trait a barrier to the evolution of generalism in this system. This study highlights that the shape of between-host trade-offs can be very heterogeneous across parasite traits, so that only some traits are pivotal to specialization.

evolutionary biology↗

bioRxiv2018

Cost of resistance: an unreasonably expensive concept

This preprint has been reviewed and recommended by Peer Community In Evolutionary Biology (https://doi.org/10.24072/pci.evolbiol.100052). The cost of resistance, or the fitness effect of resistance mutation in absence of the drug, is a very widepsread concept in evolutionary genetics and beyond. It has represented an important addition to the simplistic view that resistance mutations should solely be considered as beneficial mutations. Yet, this concept also entails a series of serious difficulties in its definition, interpretation and current usage. In many cases, it may be simpler, clearer, and more insightful to study, measure and analyze the fitness effects of mutations across environments and to better distinguish those effects from pleiotropic effects of those mutations.

evolutionary biology↗

bioRxiv2018

Decomposing parasite fitness in a two-host, two-parasite system reveals the underpinnings of parasite specialization

AO_SCPLOWBSTRACTC_SCPLOWThe ecological specialization of parasites - whether they can obtain high fitness on very few or very many different host species - is a determining feature of their ecology. In order to properly assess specialization, it is imperative to measure parasite fitness across host species; to understand its origins, fitness must be decomposed into the underlying traits. Despite the omnipresence of parasites with multiple hosts, very few studies assess and decompose their specialization in this way. To bridge this gap, we quantified the infectivity, virulence, and transmission rate of two parasites, the horizontally transmitted microsporidians Anostracospora rigaudi and Enterocytospora artemiae, in their natural hosts, the brine shrimp Artemia parthenogenetica and Artemia franciscana. Our results demonstrate that each parasite performs well on one of the two host species (A. rigaudi on A. parthenogenetica, and E. artemiae on A. franciscana), and poorly on the other. This partial specialization is driven by high infectivity and transmission rates in the preferred host, and is associated with maladaptive virulence and large costs of resistance in the other. Our study represents a rare empirical contribution to the study of parasite evolution in multi-host systems, highlighting the negative effects of under- and over-exploitation when adapting to multiple hosts.

evolutionary biology↗

bioRxiv2018

Long-term prevalence data reveals spillover dynamics in a multi-host (Artemia), multi-parasite (Microsporidia) community

In the study of multi-host parasites, it is often found that host species contribute asymmetrically to parasite transmission, with cascading effects on parasite dynamics and overall community structure. Yet, identifying which of the host species contribute to parasite transmission and maintenance is a recurring challenge. Here, we approach this issue by taking advantage of natural variation in the community composition of host species. We studied the horizontally transmitted microsporidians Anostracospora rigaudi and Enterocytospora artemiae in a Southern French metacommunity of their brine shrimp hosts, Artemia franciscana and Artemia parthenogenetica. Within the metacommunity, patches can contain either or both of the Artemia host species, so that long-term prevalence data can provide a direct link between the presence of the two host species and the persistence of the two parasites. First, we show that the microsporidian A. rigaudi is a spillover parasite: it was unable to persist in the absence of its maintenance host A. parthenogenetica. This result was particularly striking in light of A. rigaudis high prevalence (in the field) and high infectivity (when tested in the lab) in both hosts. Moreover, A. parthenogeneticas seasonal presence imposed seasonality on the rate of spillover, causing cyclical pseudo-endemics in the spillover host A. franciscana. Second, while our prevalence data was sufficient to identify E. artemiae as either a spillover or a facultative multi-host parasite, we could not distinguish between the two possibilities. This study supports the importance of studying the community context of multi-host parasites, and demonstrates that in appropriate multi-host systems, sampling across a range of conditions and host communities can lead to clear conclusions about the drivers of parasite persistence.

ecology↗