Biology subjects

van den Heuvel, J.

Publications and source records attributed to van den Heuvel, J..

At least 19 recordsLinked to original sources

bioRxiv2026

Local population genetic structure of Andrena flavipes (Hymenoptera, Andrenidae), a nest-philopatric communal mining bee, reveals isolation-by-distance and high inbreeding

Wild bee populations are declining globally and understanding how species-intrinsic traits like nest-philopatry shape local population genetic structure is increasingly important for their conservation. However, few studies have explored this at local spatial scales. To fill this gap, we used SNPs in the nuclear vitellogenin (Vg) gene to assess the local population structure and genetic diversity of the philopatric yellow-legged mining bee, Andrena flavipes, in the Netherlands, one of the most fragmented and urbanized countries in Europe. We investigated whether its reported nest-philopatry, combined with a fragmented landscape, would lead to genetic differentiation and isolation-by-distance (IBD) between populations, and low genetic diversity and inbreeding within populations. A total of 144 A. flavipes bees were sequenced for the full-length Vg gene and genotyped for SNPs. Despite high overall genetic variation, we found a heterozygote deficit and positive inbreeding coefficient in most populations, suggesting non-random mating. Low genetic differentiation was detected between populations, with no distinct genetic clusters, but with a pattern of IBD. These results suggest extensive but spatially structured gene flow, consistent with philopatric behaviour, and indicate that increasing isolation between nest-aggregations potentially leads to genetic differentiation over time. Our findings demonstrate that even in a common and widespread species, nest-philopatry and landscape fragmentation can drive inbreeding and spatially structured gene flow at local scales, highlighting the importance of maintaining habitat connectivity and semi-natural elements in agricultural and urbanized landscapes to sustain wild bee populations.

genetics↗

bioRxiv2025

Bombus terrestris Complementary Sex Determiner (BtCSD) is identified as a conserved hymenopteran sex determination region: evolution, breeding, and conservation implications

All Hymenoptera (bees, sawflies, ants, wasps) are haplodiploid. Haploid males develop from unfertilized eggs and diploid females from fertilized eggs. Many species also have single locus complementary sex determination (sl-CSD): hemizygosity of a CSD gene results in normal males and heterozygosity in normal females, but homozygosity typically yields sterile diploid males. Populations that lose CSD allelic diversity to critical level, increasingly produce detrimental diploid males. Emblematic of this problem are the bumblebees. Bumblebees are one of the fastest declining animal groups worldwide, with CSD diversity loss playing a likely role, especially in isolated populations. Presently utilized and potential future species in agriculture are also challenged by diploid males in production. Population management of both requires exact knowledge of the CSD locus. Here we report the identity of Bombus terrestris CSD, a bumblebee model that is also a major commercial pollinator. As CSD must be reciprocally homozygous in diploid males and heterozygous in diploid females, we whole-genome-sequenced these for four colonies. From this, we identified B. terrestris CSD (BtCSD) on Chromosome 2: a 26 Kb region with a long non-coding RNA region (lncRNA) and a proximate hypervariable region. Comparative analyses indicated conservation of this region across infraorder Aculeata, including other bumblebees, mason bees, and ants. This supports a deep-rooted ancestral origin for BtCSD despite a lack of homology with con-familial honey bee csd and rapid evolutionary divergence of insect sex determination cascades. Our analyses do not support the lncRNA region as functional CSD, as proposed for other taxa, because of inadequate variation to constitute distinct alleles. Rather, a downstream region is implicated for its massive structural variation and candidate coding genes including Creld and two copies of aCOP. We discuss how this identification of BtCSD has critical implications for hymenopteran evolution and bumblebee population management.

genomics↗

bioRxiv2025

Gain and loss of gene function shaped the nickel hyperaccumulation trait in Noccaea caerulescens

Nickel hyperaccumulation is an extreme adaptation to ultramafic soils observed in more than 500 plant species. However, our understanding of the molecular mechanisms underlying the evolution of this trait remains limited. To shed light on these mechanisms, we have generated a high-quality genome assembly of the metal hyperaccumulator Noccaea caerulescens. We then used this genome as reference to conduct comparative intraspecific and interspecific transcriptomic analyses using various accessions of N. caerulescens and the non-accumulating relative Microthlaspi perfoliatum, to identify genes associated with nickel hyperaccumulation. Our results suggest a correlation between nickel hyperaccumulation and a decrease in the expression of genes involved in defense responses and the regulation of membrane trafficking. Surprisingly, these analyses did not reveal a significant enrichment of genes involved in the regulation of metal homeostasis. However, we found that the expression levels of selected metal transporters, namely NcHMA3, NcHMA4 and NcIREG2, is consistently elevated in N. caerulescens accessions hyperaccumulating nickel. Furthermore, our analyses identified frameshift mutations in NcIRT1 associated with the loss of nickel hyperaccumulation in a few accessions. We further showed that the expression of a functional NcIRT1 in roots of the La Calamine accession increases nickel accumulation in shoots. Our results demonstrate that NcIRT1 participate in nickel hyperaccumulation in N. caerulescens. They also suggest that nickel hyperaccumulation is an ancient trait in N. caerulescens that has evolved from the high and constitutive expression of few metal transporters including NcIREG2 and that the trait was subsequently lost in a few accessions due to mutations in NcIRT1.

plant biology↗

bioRxiv2025

Investigating multiple types of resistance against a homing gene drive in European populations of Drosophila melanogaster

Gene drive technology may be a valuable tool for addressing several contemporary challenges, including combating disease vectors, conserving biodiversity, and controlling agricultural pests. Homing gene drives spread through a population by copying themselves onto the homologous chromosome in the germline of heterozygous individuals. However, it is possible that resistance will evolve against homing gene drives, especially if the goal is to suppress or eliminate a pest population so that resistance alleles have a large selective advantage over the gene drive. Resistance can result from a simple mutation at the drives target site, which is found in many studies but can potentially be avoided by improving drive design. However, a more complex polygenic type of resistance could also evolve through selection on standing genetic variation that affects the efficiency of the spread of the gene drive. In this study, we test an efficient homing gene drive in genetically diverse lines of Drosophila melanogaster, collected from across Europe by the DrosEU Consortium. We find that the gene drive shows considerable variability in homing efficiency, but that none of this variability can be ascribed to heritable genetic effects. Selection for complex resistance is thus unlikely and will be inefficient, probably still giving a gene drive enough time to fixate in the population. However, although our tested gene drive targets a highly conserved haploinsufficient gene with two gRNAs, we find simple resistance alleles in viable offspring. Half of these are the product of end-joining repair instead of homing and may still carry heavy fitness costs. However, the other half are the result of partial homing events. These alleles indicate that resistance could likely evolve against this gene drive in a simple, non-polygenic way. Therefore, more effective strategies may be required to address simple resistance mutations, whereas complex resistance may be unlikely to pose a substantial barrier to the employment of at least certain types of gene drive.

genetics↗

bioRxiv2024

Uncovering large effect loci and epistasis for lifespan in standing genetic variation in the fruit fly Drosophila melanogaster

Lifespan is a heritable trait with a polygenic architecture. Experimental evolution in combination with re-sequencing has often been used to identify candidate loci for lifespan in Drosophila melanogaster. Previous experiments showed that Drosophila populations experimentally evolved to increase late-life reproduction showed a correlated responses in development time, body size, but also lifespan. Subsequent whole genome sequencing allowed for the identification of candidate loci that correlated to lifespan differentiation. However, it remains difficult to assess whether candidate loci affect lifespan and to what extent such loci pleiotropically underpin multiple traits. Furthermore, recent studies indicate that lifespan effects of loci are often context dependent, but genotype-by-genotype interactions remain understudied. Therefore, here, we report on a study where we genotyped 3210 individuals for 32 candidate loci that emerged from our evolve and re-sequence experiment and tested, (1) whether these loci significantly affected lifespan, (2) the effect size of each locus, and, (3) how these loci mutually interact, i.e. determine the level of epistasis in moulding lifespan. Of the 32 loci, six showed significant main effect associations, of which three loci showed effects of 6.6 days difference in lifespan or larger, while the overall average lifespan was 41.7 days. Eight additional significant pairwise interactions between loci were found, of which four (single) main effects and one three-way interaction was significant. Lastly, we found that alleles that increased lifespan did not necessarily have higher frequencies in populations that showed increased lifespan, indicating that lifespan itself had not been the major target of selection. Our study indicates that individual genotyping following an evolve and re-sequencing study is essential to understand the mechanistic basis of polygenetic adaptation.

evolutionary biology↗

bioRxiv2024

Population genetic structure of the aphid pest Myzus persicae in organic and conventional greenhouses

Aphids display remarkable adaptability to pest control strategies and their partheno-genetic reproduction results in rapid numerical increase of higher-fitness clones. Con-sequently, a high prevalence of only a few clonal lines could indicate positive selection for these genotypes, potentially reflecting adaptation to pest control methods. Here, we investigated the clonal diversity and population genetic structure of the green peach aphid Myzus persicae using microsatellite markers, in both organic and conventionally managed Dutch sweet pepper greenhouses over four consecutive years. In total, 26 distinct multilocus genotypes (MLG) were detected, with higher clonal diversity in organic than in conventional greenhouses. Strikingly, a single MLG dominated conventional greenhouses in 2019, only to be completely replaced by a new dominant MLG by 2022. Whole-genome sequencing of 15 sampled lines -- seven sharing the same MLG and eighth with unique MLGs -- revealed that all aphids with the dominant MLG of 2019, collected from various locations and over multiple years, originated from a single parthenogenetic ancestor. Our findings indicate that the population genetic structure of M. persicae differs between organically and conventionally managed sweet pepper greenhouses. The presence of dominant MLGs in conventional crop systems may suggest positive selection or evolutionary forces such as a founder effect. Understanding the forces driving these differences in population genetic structure and their impact on the efficacy of biocontrol agents will further help us improve control strategies for M. persicae in greenhouse crops.

genetics↗

bioRxiv2024

Microbial interactions affect the tempo and mode of antibiotic resistance evolution

The global rise of antibiotic resistance impedes the treatment of bacterial infections. To limit the emergence and evolution of antibiotic resistance it is important to understand how bacterial interactions in multispecies communities affect the course of evolution. We investigated how ecological interactions between microbes derived from polymicrobial urinary tract infections affect the tempo and mode of antibiotic resistance evolution. We show that for representative strains of three uropathogens, Escherichia coli, Klebsiella pneumoniae and Enterococcus faecium, the rate and evolutionary trajectories towards antibiotic resistance differ depending on the conditioned medium mediated interactions with other microbes that alter their growth and antibiotic tolerance. Replicate lineages of the same species evolved under similar ecological conditions show parallel evolutionary trajectories, and resistance mutations and other functional targets selected differed between these conditions. Our findings demonstrate that bacterial interactions differentially affect the evolutionary potential of antibiotic resistance evolution.

ecology↗

bioRxiv2023

Improving the suppressive power of homing gene drive by co-targeting a distant-site female fertility gene

Gene drive technology has the potential to address major biological challenges, including the management of disease vectors, invasive species, and agricultural pests. After releasing individuals carrying the gene drive in the target population, suppression gene drives are designed to spread at a rapid rate and carry a recessive fitness cost, thus bringing about a decline in population size or even complete suppression. Well-studied homing suppression drives have been shown to be highly efficient in Anopheles mosquitoes and were successful in eliminating large cage populations. However, for other organisms, including Aedes mosquitoes, homing gene drives are so far too inefficient to achieve complete population suppression, mainly due to lower rates of drive conversion, which is the rate at which wild type alleles are converted into drive alleles. Low drive conversion is also a major issue in vertebrates, as indicated by experiments in mice. To tackle this issue, we propose a novel gene drive design that has two targets: a homing site where the drive is located and drive conversion takes place (with rescue for an essential gene), and a distant site for providing the fitness cost for population suppression (preferably a female fertility gene, for which no rescue is provided). We modeled this design and found that the two-target system allows suppression to occur over a much wider range of drive conversion efficiency. Specifically, in the new design, the suppressive power depends mostly on total gRNA cutting efficiency instead of just drive conversion efficiency, which is advantageous because cut rates are often substantially higher than drive conversion rates. We constructed a proof of concept in Drosophila melanogaster and show that both components of the gene drive function successfully. However, embryo drive activity from maternally deposited Cas9 as well as fitness costs for female drive heterozygotes both remain significant challenges for two-target and standard suppression drives. Overall, our improved gene drive design eases the development of strong homing suppression gene drives for many species where drive conversion is less efficient.

genetics↗

bioRxiv2023

The Cytomegalovirus M35 Protein Modulates Transcription of Ifnb1 and Other IRF3-Driven Genes by Direct Promoter Binding

Induction of type I interferon (IFN) gene expression is among the first lines of cellular defence a virus encounters during primary infection. We previously identified the tegument protein M35 of murine cytomegalovirus (MCMV) as an essential antagonist of this antiviral system. M35 localizes to the nucleus and interferes with type I IFN induction downstream of pattern-recognition receptor (PRR) activation. Here, we report structural and mechanistic details of M35s function. Using electrophoretic mobility shift assays (EMSA), we demonstrate that purified M35 protein specifically binds to the regulatory DNA element that governs transcription of the first type I IFN gene induced in non-immune cells, Ifnb1. Determination of M35s crystal structure combined with reverse genetics revealed that homodimerisation is a key feature for M35s immunomodulatory activity. DNA-binding sites of M35 overlapped with the recognition elements of interferon regulatory factor 3 (IRF3), a key transcription factor activated by PRR signalling. Chromatin immunoprecipitation (ChIP) showed reduced binding of IRF3 to the host Ifnb1 promoter in the presence of M35. We furthermore defined the IRF3-dependent and the type I IFN signalling-responsive genes in murine fibroblasts by RNA sequencing of metabolically labelled transcripts (SLAM-seq), and assessed M35s global effect on gene expression. Stable expression of M35 broadly influenced the transcriptome in untreated cells and specifically down-regulated basal expression of IRF3-dependent genes, and during MCMV infection, M35 impaired expression of IRF3-responsive genes aside of Ifnb1. Our results suggest that M35-DNA binding directly antagonises gene induction by IRF3 and impairs the antiviral response more broadly than formerly recognised. ImportanceReplication of the ubiquitous human cytomegalovirus (CMV) in healthy individuals mostly goes unnoticed, but can impair foetal development or cause life-threatening symptoms in immunosuppressed or -deficient patients. Like other herpesviruses, CMV extensively manipulates its hosts and establishes lifelong latent infections. Murine CMV (MCMV) presents an important model system as it allows the study of CMV infection in the host organism. We previously showed that during entry, MCMV virions release the evolutionary conserved protein M35 protein to immediately dampen the antiviral type I interferon (IFN) response induced by pathogen detection. Here we show that M35 dimers bind to regulatory DNA elements and interfere with recruitment of interferon regulatory factor 3 (IRF3), a key factor for antiviral gene expression. Thereby, M35 interferes with expression of type I IFNs and other IRF3-dependent genes. Unrelated proteins from other herpesviruses employ the same mechanism, reflecting the importance for herpesviruses to avoid IRF3-mediated gene induction.

molecular biology↗

bioRxiv2023

The long-term effects of genomic selection: 2. Changes in allele frequencies of causal loci and new mutations

Genomic selection has become the dominant tool for genetic improvement in livestock and plants. Therefore, its sustainability is essential for global food production. Selection changes the allelic architecture of traits to create genetic gain. It remains unknown whether the changes in allele architecture are different for genomic selection and whether they depend on the genetic architectures of traits. Here we investigate the allele frequency changes of loci and new causal mutations under fifty generations of phenotypic, pedigree, and genomic selection, for a trait controlled by either additive, additive and dominance, or additive, dominance and epistatic effects. Genomic selection resulted in slightly larger and faster changes in allele frequencies of causal loci than pedigree selection. For each locus, allele frequency change per generation was not only influenced by its statistical additive effect, but also by the linkage phase with other loci and its allele frequency. Selection fixed a large number of loci, and five times more unfavorable alleles became fixed with genomic and pedigree selection than with phenotypic selection. For pedigree selection, this was mainly a result of increased genetic drift, while genetic hitchhiking had a large effect with genomic selection. When epistasis was present, the average allele frequency change was smaller ([~]15% lower) and a lower number of loci became fixed for all selection methods. We conclude that for long-term genetic improvement, it is very important to be able to minimize the impact of hitchhiking and to limit the loss of favorable alleles more that current genomic selection methods do.

genetics↗

bioRxiv2022

Identification of heterokaryon incompatibility genes in Aspergillus fumigatus highlights a narrow footprint of ancient balancing selection

In fungi, a phenomenon termed heterokaryon incompatibility restricts hyphal fusion to occur within an individual since fusion between individuals leads to cell death. Generally, the genes involved are found to be under balancing selection from negative frequency dependent fitness. Here, we assess this in Aspergillus fumigatus, a human pathogenic fungus with an extremely high crossover rate. Using auxotrophic markers we screened sexual progeny for compatibility to identify genes involved in this process, the so-called het genes. In total, 5/148 (3.4%) offspring were compatible with a parent and 166/2142 (7.7%) sibling pairs were compatible, consistent with several segregating incompatibility loci. Genetic mapping resulted in five loci, four of which could be fine mapped to individual genes, of which we tested three through heterologous expression, confirming their causal relationship. Surprisingly, a population-level analysis of two available independent datasets did not show an increase in Tajimas D near these loci, normally a hallmark of balancing selection. However, analysis of closely related species did show trans-species polymorphisms across >10 million years, and equal allele frequencies within A. fumigatus. Using available de novo assemblies, we show that these balanced polymorphisms are restricted to within several hundred base pairs flanking the coding sequence, potentially due to this species high crossover rate. In addition to identifying the first het genes in an Aspergillus species, this work highlights the interaction of long-term balancing selection with a high recombination rate. Future mechanistic work on these het genes may provide novel routes for clinical therapies, as well as opportunities for strain improvement in biotechnology.

evolutionary biology↗

bioRxiv2022

Meiosis in the human pathogen Aspergillus fumigatus has the highest known number of crossovers

Evidence from both population genetics and a laboratory sexual cycle indicate that sex is common in the fungus Aspergillus fumigatus. However, the impact of sexual reproduction has remained unclear. Here, we show that meiosis in A. fumigatus involves the highest known recombination rate, producing ~29 crossovers per chromosome. This represents the highest known crossover rate for any Eukaryotic species. We validate this recombination rate by mapping resistance to acriflavine, a common genetic marker. We further show that this recombination rate can produce the commonly encountered TR34/L98H azole-resistant cyp51A haplotype in each sexual event, facilitating its rapid and global spread. Understanding the consequences of this unparalleled crossover rate will not only enrich our genetic understanding of this emergent human pathogen, but of meiosis in general. One-Sentence SummaryGenetic exchange between chromosomes during sex in Aspergillus fumigatus is higher than in any other known organism.

genetics↗

bioRxiv2021

Conversion rate to the secondary conformation state in the binding mode of SARS-CoV-2 spike protein to human ACE2 may predict infectivity efficacy of the underlying virus mutant

Since its outbreak in 2019 SARS-CoV-2 has spread with high transmission efficiency across the world, putting health care as well as economic systems under pressure [1, 2]. During the course of the pandemic, the originally identified SARS-CoV-2 variant has been widely replaced by various mutant versions, which showed enhanced fitness due to increased infection and transmission rates [3, 4]. In order to find an explanation, why SARS-CoV-2 and its emerging mutated versions showed enhanced transfection efficiency as compared to SARS-CoV 2002, an improved binding affinity of the spike protein to human ACE has been proposed by crystal structure analysis and was identified in cell culture models [5-7]. Kinetic analysis of the interaction of various spike protein constructs with the human ACE2 was considered to be best described by a Langmuir based 1:1 stoichiometric interaction. However, we demonstrate in this report that the SARS-CoV-2 spike protein interaction with ACE2 is best described by a two-step interaction, which is defined by an initial binding event followed by a slower secondary rate transition that enhances the stability of the complex by a factor of [~]190 with an overall KD of 0.20 nM. In addition, we show that the secondary rate transition is not only present in SARS-CoV-2 wt but is also found in B.1.1.7 where its transition rate is five-fold increased.

molecular biology↗

bioRxiv2021

Processing of the Ribosomal Ubiquitin-Like Fusion Protein FUBI-eS30/FAU is Required for 40S Maturation and Depends on USP36

In humans and other holozoan organisms, the ribosomal protein eS30 is synthesized as a fusion protein with the ubiquitin-like protein FUBI. However, FUBI is not part of the mature 40S ribosomal subunit and cleaved off by an as-of-yet unidentified protease. How FUBI-eS30 processing is coordinated with 40S subunit maturation is unknown. To study the mechanism and importance of FUBI-eS30 processing, we expressed non-cleavable mutants in human cells, which affected late steps of cytoplasmic 40S maturation, including the maturation of 18S rRNA and recycling of late-acting ribosome biogenesis factors. Differential affinity purification of wild-type and non-cleavable FUBI-eS30 mutants identified the deubiquitinase USP36 as a candidate FUBI-eS30 processing enzyme. Depletion of USP36 by RNAi or CRISPRi indeed impaired FUBI-eS30 processing and moreover, purified USP36 cut FUBI-eS30 in vitro. Together, these data demonstrate the functional importance of FUBI-eS30 cleavage and identify USP36 as a novel protease involved in this process.

cell biology↗

bioRxiv2021

The long-term effects of genomic selection: Response to selection, additive genetic variance and genetic architecture

Genomic selection has revolutionized genetic improvement in animals and plants, but little is known of its long term effects. Here we investigate the long-term effects of genomic selection on the change in the genetic architecture of traits over generations. We defined the genetic architecture as the subset, allele frequencies and statistical additive effects of causal loci. We simulated a livestock population under 50 generations of phenotypic, pedigree, or genomic selection for a single trait, controlled by either only additive, additive and dominance, or additive, dominance and epistatic effects. The simulated epistasis was based on yeast data. The observed change in genetic architecture over generations was similar for genomic and pedigree selection, and slightly smaller for phenotypic selection. Short-term response was highest with genomic selection, while long-term response was highest with phenotypic selection, especially when non-additive effects were present. This was mainly because the loss in genetic variance and in segregating loci was much greater with genomic selection. Compared to pedigree selection, genomic selection lost a similar amount of the genetic variance but maintained more segregating loci, which on average had lower minor allele frequencies. For all selection methods, the presence of epistasis limited the changes in allele frequency and the fixation of causal loci, and substantially changed the statistical additive effects over generations. Our results show that non-additive effects can have a substantial impact on the change in genetic architecture. Therefore, non-additive effects can substantially impact the accuracy and future genetic gain of genomic selection.

genetics↗

bioRxiv2020

Somatic deficiency causes reproductive parasitism in a fungus

Some multicellular organisms can fuse because mergers potentially provide mutual benefits. However, experimental evolution in the fungus Neurospora crassa has demonstrated that free fusion of mycelia favours cheater lineages, but the mechanism and evolutionary dynamics of dishonest exploitation are unknown. Here we show, paradoxically, that all convergently evolved cheater lineages have similar fusion deficiencies. These mutants are unable to initiate fusion but retain access to wild-type mycelia that fuse with them. This asymmetry reduces cheater-mutant contributions to somatic substrate-bound hyphal networks, but increases representation of their nuclei in the aerial reproductive hyphae. Cheaters only benefit when relatively rare and likely impose genetic load reminiscent of germline senescence. We show that the consequences of somatic fusion can be unequally distributed among fusion partners, with the passive non-fusing partner profiting more. We discuss how our findings may relate to the extensive variation in fusion frequency of fungi found in nature.

evolutionary biology↗

bioRxiv2020

Braconidae revisited: Bracon brevicornis genome showcases the potential of linked-read sequencing in identifying a putative complementary sex determiner gene

Bracon brevicornis is an ectoparasitoid of a wide range of larval-stage Lepidopterans, including several pests of important crops, such as the corn borer, Ostrinia nubilalis. It is also one of the earliest documented cases of complementary sex determination in Hymenoptera. Here, we present the linked-read genome of B. brevicornis, complete with an ab initio-derived annotation and protein comparisons with fellow braconids, Fopius arisanus and Diachasma alloem. We demonstrate the potential of linked-read assemblies in exploring regions of heterozygosity and search for structural and homology-derived evidence of the complementary sex determiner gene (csd).

genomics↗

bioRxiv2020

Genomics of sex allocation in the parasitoid wasp Nasonia vitripennis

BackgroundWhilst adaptive facultative sex allocation has been widely studied at the phenotypic level across a broad range of organisms, we still know remarkably little about its genetic architecture. Here, we explore the genome-wide basis of sex ratio variation in the parasitoid wasp Nasonia vitripennis, perhaps the best studied organism in terms of sex allocation, and well known for its response to local mate competition (LMC). ResultsWe performed a genome-wide association study (GWAS) for single foundress sex ratios using iso-female lines derived from the recently developed outbred N. vitripennis laboratory strain HVRx. The iso-female lines capture a sample of the genetic variation in HVRx and we present them as the first iteration of the Nasonia vitripennis Genome Reference Panel (NVGRP 1.0). This panel provides an assessment of the standing genetic variation for sex ratio in the study population. Using the NVGRP, we discovered a cluster of 18 linked SNPs, encompassing 9 annotated loci associated with sex ratio variation. Furthermore, we found evidence that sex ratio has a shared genetic basis with clutch size on three different chromosomes. ConclusionsOur approach provides a thorough description of the quantitative genetic basis of sex ratio variation in Nasonia at the genome level and reveals a number of inter-related candidate loci underlying sex allocation regulation.

evolutionary biology↗