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Evans, D. M.

Publications and source records attributed to Evans, D. M..

At least 19 recordsLinked to original sources

Revealing parasitoid-pest interactions using multi-marker metabarcoding: a nationwide assessment of parasitism in cabbage stem flea beetle larvae

Management of insect pests of oilseed rape (Brassica napus L.) such as cabbage stem flea beetle (CSFB; Psylliodes chrysocephala L.) is increasingly challenging given a lack of effective permitted insecticides. Conservation biocontrol, including through naturally-occurring parasitoids of CSFB, is one of the first lines of defense and the baseline for integrated pest management (IPM) strategies, but we lack a comprehensive understanding of the parasitoids involved and how parasitism rates vary regionally. Such data have traditionally required rearing of parasitoids from their pest hosts, which is highly error-prone, laborious and overlooks instances of multiple parasitism and hyperparasitism. Using multi-marker DNA metabarcoding, including a novel host-exclusion parasitoid PCR primer pair, we assessed parasitism of 1,040 CSFB larvae from 13 counties in England, UK. We confidently identified seven parasitoids of CSFB larvae, with ten taxa present in unfiltered data. Parasitism rates differed between regions, with the north of England having significantly lower parasitism rates than southern regions. Our novel beetle parasitoid PCR primers demonstrate a high congruence with visual detections of parasitoids and a high rate of novel interaction detections. Ultimately, by determining both rates of parasitism and natural enemy identities, these data significantly extend our understanding of in-field CSFB parasitoid community dynamics. This information could guide the enhancement of farm management, especially using network science in decision support systems related to insecticide application, but also more broadly in the context of crop and habitat management for improved conservation biocontrol and IPM.

ecology↗

The impacts of grazing pressure by large herbivores on short-tailed field vole (Microtus agrestis) population cycles: results from a long-term upland experiment

Understanding how large herbivores influence cyclic small-mammal populations is essential for predicting community dynamics in grazed ecosystems. Using a 23-year upland grazing experiment in Scotland, United Kingdom, we test how varying livestock grazing pressures affect population cycles of the short-tailed field vole Microtus agrestis, a keystone herbivore and prey species of birds of conservation concern. We combined long-term vole sign indices (VSI), vegetation surveys, climate data and used wavelet analyses and mixed-effects models to quantify changes in VSI (a proxy for abundance), cycle amplitude and periodicity across four grazing treatments and three spatial blocks. Vole abundance and cycle amplitude declined with increasing grazing pressure, yet the frequency of vole population oscillations remained strikingly consistent across all treatments, with a dominant ~3.5-year cycle persisting throughout most of the study. Ungrazed plots supported the highest mean VSI and the largest amplitude oscillations. We found a pronounced, spatially-restricted cycle collapse occurred between 2009-2016 in one experimental block. This breakdown coincided with unusually cold winters and lower vegetation density, suggesting that local microclimate and habitat structure interact to destabilise vole cycles. Vegetation density (but not height) predicted VSI in the more intensively grazed treatments, indicating that grazing-driven changes in habitat structure indirectly mediate vole dynamics. Our findings demonstrate that large herbivores can substantially modify vole population dynamics through both direct and indirect pathways, altering cycle amplitude, habitat suitability and resilience to climatic perturbations. These results highlight the need to consider interactions between grazing, vegetation structure and climate variability when predicting small-mammal population dynamics and their cascading ecological effects.

ecology↗

The genetic architecture of trabecular bone score and association with fracture: a genome-wide association and meta-analysis

BackgroundTrabecular bone score (TBS) is a texture-based measurement derived from DXA scans, which describes the distribution of mineral across the vertebral bodies. Identifying its genetic determinants is crucial for enhancing understanding of its biological basis and clarifying its relationship with fracture risk. MethodsWe conducted a large-scale genome-wide association study (GWAS) of TBS from 44,767 participants (95.08% European ancestry). Sex heterogeneity was assessed through sex-stratified GWAS. Post-GWAS analyses included functional annotation, gene-set enrichment analysis, and cis-expression quantitative trait locus (cis-eQTL) colocalization. Two-sample and multivariable Mendelian randomization (MR) were employed to investigate the causal effect of TBS on fractures. FindingsWe identified 33 independent variants associated with TBS, which explained 4.06% of TBS phenotypic variance. All the discovered signals map to previously identified BMD-associated loci. Additionally, we identified genetic variants in the RAB11FIP3 locus that exhibited a sex-heterogeneous effect, being associated with TBS exclusively in males. Functional annotation and colocalization identified functional genes related to TBS. The two-sample and multivariable MR analyses indicated that TBS potentially has an independent causal effect on fracture risk. InterpretationOur study unveiled 33 independent loci associated with TBS, all in BMD-associated loci. One locus was further identified as associated with TBS only in males. MR results suggested that genetically derived TBS may be causally associated with fracture risk at different sites, potentially beyond BMD. This study provides insights into the TBS genetic architecture and uncovers its potential clinical applications in fracture risk prediction. FundingAll funding information can be found in the Acknowledgements section. Research in contextO_ST_ABSEvidence before this studyC_ST_ABSOsteoporosis is a common disease prevalent in older adults, mainly diagnosed by low bone mineral density and disruption of bone architecture. While the genetic determinants of bone mass have been well studied, the genetic architecture of bone features beyond BMD remains largely unknown. Added value of this studyThis study presents a large genome-wide association meta-analysis of the trabecular bone score (TBS), a measurement of trabecular distribution of bone mineralization across vertebral bodies. Our study identified 33 independent variants associated with TBS and one association signal only in males. Functional annotation highlighted crucial genes related to TBS. The two-sample and multivariable Mendelian randomization (MR) analyses suggested that TBS may be causally linked with fracture risk, potentially independent of BMD. Implications of all the available evidenceOur study represents an expansion of the traditional bone density phenotype used in most previous skeletal genetic studies. Based on the findings that all of the significant loci for TBS have been previously identified in GWAS of BMD, we conclude that TBS-associated variants have pleiotropic effects affecting not only mineral density but also the distribution patterns of minerals in the cancellous bone. Continuing to perform genetic studies of new skeletal phenotypes beyond BMD could ultimately impact the management and prediction of osteoporosis patients.

genomics↗

Germline sequence variation within the ribosomal DNA is associated with human complex traits

The ribosome is one of the core macromolecules in the cell. The ribosomal RNAs (rRNA), which are essential components of the ribosome, are coded by the multi-copy ribosomal DNA (rDNA). Despite its highly conserved function, the rDNA displays substantial variation within all species analysed to date. This variation comprises both inter-individual differences in total copy number (CN) as well as inter- and intragenomic sequence variation in the form of single nucleotide variants (SNV) and insertions/deletions (INDELs) across rDNA copies. Whether germline variation of rDNA sequence associates with phenotypic traits in humans is, to date, unknown. Here, using the UK Biobank whole genome sequencing data, we first derive a high confidence list of rDNA-associated SNVs and INDELs that we validate in multiple ways. Using this list, we show that specific rDNA variants associate with several human traits. In particular, traits associated with body size appear enriched in variants within the Expansion Segment 15L region in the 28S rRNA. The strength of these associations does not diminish when accounting for the total rDNA CN of each individual. Our work represents the first large-scale association analysis of human traits with germline sequence variation in the rDNA, a source of human complex trait-relevant genetic variation that has thus far been largely ignored.

genetics↗

Multiscale analysis and functional validation of the cellular and genetic determinants of skeletal disease

Musculoskeletal diseases are a major health burden. Development of bone-active therapies has been hindered by limited understanding of the cells and genes that regulate the skeleton. We exploited the value of cross-species analysis and developed single-cell methodologies in skeletal tissues to define the critical endosteal compartment that regulates bone turnover. Thirty-four distinct cell types were identified, and disease-relevant cells prioritised by enrichment for rare skeletal disorder genes and bone mineral density-associated genes in an extended UK Biobank GWAS. Functional validation was undertaken in over one thousand genetically modified mouse models. Endothelial and vascular smooth muscle cells were identified as novel skeletal disease-relevant cells alongside osteoblast, chondrocyte and osteoclast cell lineages. Hundreds of cell-specific genes with unappreciated roles in skeletal pathophysiology were identified. This comprehensive cellular and molecular framework underpins skeletal physiology and disease, and will help prioritise new therapeutic targets to accelerate development of novel therapies to treat musculoskeletal disease.

genetics↗

Partitioning genetic effects on birth weight at classical human leukocyte antigen loci into indirect maternal and direct fetal components using structural equation modelling

Birth weight (BW), as a proxy for intrauterine growth, is influenced by both fetal and maternal genetic factors. Single nucleotide polymorphisms in the human leukocyte antigen (HLA) region in both maternal and fetal genomes have been robustly associated with BW in previous genetic association studies suggesting the involvement of classical HLA alleles in BW etiology. However, no study to date has partitioned the association between BW and classical HLA alleles into maternal and fetal components. We used structural equation modelling (SEM) to estimate the indirect maternal (i.e. via the intrauterine environment) and direct fetal effects of classical HLA alleles on BW. Our SEM leverages the data structure of the UK Biobank (UKB), which includes participants own BW and/or the BW of their firstborn child (in the case of UKB females). We show via simulation that our model yields asymptotically unbiased estimates of the maternal and fetal allelic effects on BW and appropriate type I error rates, in contrast to simple regression models that estimate unconditioned maternal and fetal effects. Asymptotic power calculations show that we have sufficient power to detect moderate-sized maternal or fetal allelic effects (standardized effect size [≥] 0.01) of common HLA alleles on BW in the UKB. Applying our SEM to imputed classical HLA alleles and own and offspring BW of [~]270,000 participants from the UKB replicated the previously reported association at the HLA-C locus (C*04:01, P = 2.13x10-7, C*05:01, P= 6.91x10-5, C*03:03, P= 4.53x10-3, respectively) and revealed strong evidence for maternal (HLA-A*03:01, P = 7.90x10-8; B*35:01, P = 7.78x10-5; B*39:06, P = 8.49 x10-5) and fetal allelic effects (HLA-B*39:06, P = 4.03x10-4) of non-HLA-C alleles on BW. These novel allelic associations between BW and classical HLA alleles provide insight into the immunogenetics of fetal growth in utero.

genetics↗

Using adopted individuals to partition maternal genetic effects into prenatal and postnatal effects on offspring phenotypes

Maternal genetic effects can be defined as the effect of a mothers genotype on the phenotype of her offspring, independent of the offsprings genotype. Maternal genetic effects can act via the intrauterine environment during pregnancy and/or via the postnatal environment. In this manuscript, we present a simple extension to the basic adoption design that uses structural equation modelling (SEM) to partition maternal genetic effects into prenatal and postnatal effects. We assume that in biological families, offspring phenotypes are influenced prenatally by their mothers genotype and postnatally by both parents genotypes, whereas adopted individuals phenotypes are influenced prenatally by their biological mothers genotype and postnatally by their adoptive parents genotypes. Our SEM framework allows us to model the (potentially) unobserved genotypes of biological and adoptive parents as latent variables, permitting us in principle to leverage the thousands of adopted singleton individuals in the UK Biobank. We examine the power, utility and type I error rate of our model using simulations and asymptotic power calculations. We apply our model to polygenic scores of educational attainment and birth weight associated variants, in up to 5178 adopted singletons, 983 trios, 3650 mother-offspring pairs, 1665 father-offspring pairs and 350330 singletons from the UK Biobank. Our results show the expected pattern of maternal genetic effects on offspring birth weight, but unexpectedly large prenatal maternal genetic effects on offspring educational attainment. Sensitivity and simulation analyses suggest this result may be at least partially due to adopted individuals in the UK Biobank being raised by their biological relatives. We show that accurate modelling of these sorts of cryptic relationships is sufficient to bring type I error rate under control and produce unbiased estimates of prenatal and postnatal maternal genetic effects. We conclude that there would be considerable value in following up adopted individuals in the UK Biobank to determine whether they were raised by their biological relatives, and if so, to precisely ascertain the nature of these relationships. These adopted individuals could then be incorporated into informative statistical genetics models like the one described in our manuscript to further elucidate the genetic architecture of complex traits and diseases.

genetics↗

Estimating direct and indirect genetic effects on offspring phenotypes using genome-wide summary results data: a comparison of multivariate methods

Estimation of the direct genetic effect of an individuals own genotype on their phenotype, independent of any contaminating indirect parental genetic effects is becoming increasingly important. These conditional estimates are of interest in their own right, but are also useful for downstream analyses such as intergenerational Mendelian randomization. We compare several available multivariate methods that utilize summary results statistics from genome-wide association studies to determine how well they estimate conditional direct and indirect genetic effects, while accounting for sample overlap. Using robustly associated birth weight variants and data from the UK Biobank, we contrasted the point estimates and their standard errors at each of the individual loci compared to those obtained using individual level genotype data, in addition to comparing the computational time, inflation of the test statistics and number of genome-wide significant SNPs identified by each of the methods. We show that Genomic SEM outperforms the other methods in accurately estimating conditional genetic effects and their standard errors. We subsequently applied Genomic SEM to fertility data in the UK Biobank and partitioned the genetic effect into female and male fertility in addition to a sibling specific effect. This analysis identified one novel locus for fertility and replicated seven previously identified loci. We also identified genetic correlations between fertility and educational attainment, risk taking behaviour, autism and subjective well-being. We therefore recommend Genomic SEM to be used to partition genetic effects across the genome into direct and indirect components.

genetics↗

Fetal alleles predisposing to metabolically favourable adiposity are associated with higher birth weight

BackgroundHigher birth weight is associated with higher adult body mass index (BMI). If genetic variants can be identified with alleles that predispose to both greater fetal growth and to greater adult adiposity, such shared genetic effects might indicate biological processes important in the early patterning of adiposity. However, variants identified in genome-wide association studies of adult BMI have overall been only weakly associated with birth weight. Genetic variants have recently been identified where one allele is associated with higher adult body fat percentage, but lower risk of metabolic disease, likely due to a favourable body fat distribution. The effect of these adult metabolically favourable adiposity alleles on an individuals own birth weight is unknown. AimWe aimed to test the effect on birth weight of a fetal genetic predisposition to higher metabolically favourable adult adiposity and to compare this with the effects of a fetal genetic predisposition to higher adult BMI. We also aimed to examine the effects of a genetic predisposition to higher metabolically favourable adult adiposity or BMI on other birth anthropometric traits (length, ponderal index, head circumference and skinfold thickness) and on cord-blood insulin, leptin and adiponectin. MethodsWe used published GWAS data from up to 406,063 individuals to estimate the fetal effects on birth weight of alleles that are robustly associated with higher metabolically favourable adult adiposity or BMI. We additionally used 9,350 mother-child pairs from four cohorts to test the effects of the same alleles on other birth anthropometric traits and cord-blood markers. In all analyses, we adjusted for potential confounding due to the maternal genotype. We used inverse-variance weighted meta-analyses to combine summary data across SNPs. ResultsFetal genetic predisposition to higher metabolically favourable adult adiposity was associated with higher birth weight (10 grams (95% CI: 7 to 13) higher mean birth weight per 1 SD pooled "genetic score"). Fetal genetic predisposition to higher adult BMI was also associated with higher birth weight, but with a smaller magnitude of effect (4 grams (95% CI: 0 to 8) higher mean birth weight per 1 SD pooled "genetic score") and with higher heterogeneity across SNPs. Effects on other birth anthropometric outcomes were consistent with the effect on birth weight but with wider confidence intervals. There was no strong evidence for an effect on cord-blood markers. ConclusionsSome genetic variants previously linked to adult adiposity influence birth weight. Alleles that predispose to higher metabolically favourable adult adiposity collectively have a stronger effect on birth weight than those predisposing to higher BMI. This suggests that the early accumulation of a metabolically favourable fat distribution might underlie part of the observed association between higher birth weight and higher adult BMI. Larger samples are needed to clarify the effects on other birth anthropometric measures and cord-blood markers.

genetics↗

Modeling Parent-Specific Genetic Nurture in Families with Missing Parental Genotypes: Application to Birthweight and BMI

Disaggregation and estimation of genetic effects from offspring and parents has long been of interest to statistical geneticists. Recently, technical and methodological advances have made the genome-wide and loci-specific estimation of direct offspring and parental genetic nurture effects more possible. However, unbiased estimation using these methods requires datasets where both parents and at least one child have been genotyped, which are relatively scarce. Our group has recently developed a method and accompanying software (IMPISH; Hwang et al., 2020) which is able to impute missing parental genotypes from observed data on sibships and estimate their effects on an offspring phenotype conditional on the effects of genetic transmission. However, this method is unable to disentangle maternal and paternal effects, which may differ in magnitude and direction. Here, we introduce an extension to the original IMPISH routine which takes advantage of all available nuclear families to impute parent-specific missing genotypes and obtain asymptotically unbiased estimates of genetic effects on offspring phenotypes. We apply this this method to data from related individuals in the UK Biobank, showing concordance with previous estimates of maternal genetic effects on offspring birthweight. We also conduct the first GWAS jointly estimating offspring-, maternal-, and paternal-specific genetic effects on body mass index.

genetics↗

Direct and indirect effects of maternal, paternal, and offspring genotypes: Trio-GCTA

Indirect genetic effects from relatives may result in misleading quantifications of heritability, but can also be of interest in their own right. In this paper we propose Trio-GCTA, a model for separating direct and indirect genetic effects when genome-wide single nucleotide polymorphism data have been collected from parent-offspring trios. The model is applicable to phenotypes obtained from any of the family members. We discuss appropriate parameter interpretations and apply the method to four exemplar phenotypes; offspring birth weight, offspring temperament, maternal relationship satisfaction, and paternal body-mass index, using real data from the Norwegian Mother, Father and Child Cohort Study (MoBa).

genetics↗

Haplotype-based heritability estimations reveal gestational duration as a maternal trait and fetal size measurements at birth as fetal traits in human pregnancy

AbstractGenotype-based approaches for the estimation of SNP-based narrow-sense heritability [Formula] have limited utility in pregnancy-related outcomes due to confounding by the shared alleles between mother and child. Here, we propose a haplotype-based approach to estimate the genetic variance attributable to three haplotypes - maternal transmitted [Formula], maternal non-transmitted [Formula] and paternal transmitted [Formula] in mother-child pairs. We show through extensive simulations that our haplotype-based approach outperforms the conventional and contemporary approaches for resolving the contribution of maternal and fetal effects, particularly when m1 and p1 have different effects in the offspring. We apply this approach to estimate the explicit and relative maternal-fetal genetic contribution to the phenotypic variance of gestational duration and gestational duration adjusted fetal size measurements at birth in 10,375 mother-child pairs. The results reveal that variance of gestational duration is mainly attributable to m1 and m2 ([Formula]= 17.3%, S. E. = 5.2%; [Formula] = 12.2%, S. E. = 5.2%; [Formula] = 0.0%, S. E. = 5.0%). In contrast, variance of fetal size measurements at birth are mainly attributable to m1 and p1 ([Formula] = 18.6 - 36.4%, [Formula] = 0.0 - 5.2% and [Formula] = 4.4 - 13.6%). Our results suggest that gestational duration and fetal size measurements are primarily genetically determined by the maternal and fetal genomes, respectively. In addition, a greater contribution of m1 as compared to m2 and p1 [Formula] to birth length and head circumference suggests a substantial influence of correlated maternal-fetal genetic effects on these traits. Our newly developed approach provides a direct and robust alternative for resolving explicit maternal and fetal genetic contributions to the phenotypic variance of pregnancy-related outcomes.

genetics↗

Osteocyte Transcriptome Mapping Identifies a Molecular Landscape Controlling Skeletal Homeostasis and Susceptibility to Skeletal Disease

Osteocytes are master regulators of the skeleton. We mapped the transcriptome of osteocytes from different skeletal sites, across age and sexes in mice to reveal genes and molecular programs that control this complex cellular-network. We define an osteocyte transcriptome signature of 1239 genes that distinguishes osteocytes from other cells. 77% have no previously known role in the skeleton and are enriched for genes regulating neuronal network formation, suggesting this program is important in osteocyte communication. We evaluated 19 skeletal parameters in 733 knockout mouse lines and reveal 26 osteocyte transcriptome signature genes that control bone structure and function. We showed osteocyte transcriptome signature genes are enriched for human orthologs that cause monogenic skeletal disorders (P=2.4x10-22) and are associated with the polygenic diseases osteoporosis (P=1.8x10-13) and osteoarthritis (P=1.6x10-7). Thus, we reveal the molecular landscape that regulates osteocyte network formation and function and establish the importance of osteocytes in human skeletal disease.

systems biology↗

ACE 2 Coding Variants: A Potential X-linked Risk Factor for COVID-19 Disease

Viral genetic variants are widely known to influence disease progression among infected humans. Given the recent and rapid emergence of pandemic SARS-CoV-2 infection, the cause of COVID-19 disease, viral protein variants have attracted research interest. However, little has yet been written about genetic risk factors among human hosts. Human genetic variation has proven to affect disease progression and outcome for important diseases such as HIV infection and malaria infestation. The fact that the human ACE2 protein is encoded on the X chromosome means that males who carry rare ACE2 coding variants will express those variants in all ACE2-expressing cells, whereas females will typically express those variants in a mosaic distribution determined by early X-inactivation events. This sex-based difference in ACE2 expression has unique implications for epidemiological studies designed to assess host genetic factors influencing progression from asymptomatic SARS-coV-2 infection to COVID-19. Here we present theoretical modelling of rare ACE2 coding variants documented to occur naturally in several human superpopulations and subpopulations, and show that rare variants predicted to affect the binding of ACE2 to the SARS-CoV-2 spike protein exist in people. Though the rs4646116 (p.Lys26Arg) allele is found in 1 in 70 Ashkenazi Jewish males, and in 1 in 172 non-Finnish European males, this allele is found at higher frequencies in females. Furthermore, the class of missense ACE2 alleles predicted to affect SARS-CoV-2 binding are found in aggregate among 1.43% and 2.16% of Ashkenazi males and females, respectively, as well as in 0.58% and 1.24% of European males and females outside of Finland. These alleles are rarer in other population groups, and almost absent from East Asians genotyped to date. Though we are aware that full genome-wide and exome-wide sequencing studies may ultimately be required to assess human genetic susceptibility to SARS-CoV-2 fully, we argue on the basis of strong prior probabilities that genotyping of this class of alleles is justified in cases of atypical SARS-CoV-2 diseases, such as asymptomatic super-spreaders (if any are identified), and in neonatal/paediatric-onset COVID-19 disease. Even relatively rare susceptibility factors (1% or fewer carriers) may become quantitatively important in the context of hundreds of thousands of infections. A small number of asymptomatic carriers, or a small number of super-spreaders, or a small segment of the population that is disproportionately likely to require intensive care, can magnify the medical, social and economic impacts of a pandemic of this size. The speed of the pandemic and the large number of affected cases worldwide justify efforts to identify all possible risk factors for adverse outcomes, including efforts to identify genetic susceptibility factors in human hosts.

bioinformatics↗

Estimating indirect parental genetic effects on offspring phenotypes using virtual parental genotypes derived from sibling and half sibling pairs

Indirect parental genetic effects may be defined as the influence of parental genotypes on offspring phenotypes over and above that which results from the transmission of genes from parents to children. However, given the relative paucity of large-scale family-based cohorts around the world, it is difficult to demonstrate parental genetic effects on human traits, particularly at individual loci. In this manuscript, we illustrate how parental genetic effects on offspring phenotypes, including late onset diseases, can be estimated at individual loci in principle using large-scale genome-wide association study (GWAS) data, even in the absence of parental genotypes. Our strategy involves creating "virtual" mothers and fathers by estimating the genotypic dosages of parental genotypes using physically genotyped data from relative pairs. We then utilize the expected dosages of the parents, and the actual genotypes of the offspring relative pairs, to perform conditional genetic association analyses to obtain asymptotically unbiased estimates of maternal, paternal and offspring genetic effects. We develop a freely available web application that quantifies the power of our approach using closed form asymptotic solutions. We implement our methods in a user-friendly software package IMPISH (IMputing Parental genotypes In Siblings and Half-Siblings) which allows users to quickly and efficiently impute parental genotypes across the genome in large genome-wide datasets, and then use these estimated dosages in downstream linear mixed model association analyses. We conclude that imputing parental genotypes from relative pairs may provide a useful adjunct to existing large-scale genetic studies of parents and their offspring.

genetics↗

Investigating the causal effect of maternal vitamin B12 and folate levels on offspring birthweight

Lower maternal serum vitamin B12 (B12) and folate levels have been associated with lower offspring birthweight in observational studies. The aim of this study was to investigate whether this relationship is causal. We performed two-sample Mendelian Randomization (MR) using summary data on associations between genotype-B12 (10 genetic variants) or genotype-folate (4 genetic variants) levels from a genome-wide association study of 45,576 individuals (sample 1) and maternal-specific genetic effects on offspring birthweight from the latest EGG consortium meta-analysis with 297,356 individuals reporting their own birthweight and 210,248 women reporting their offsprings birthweight (sample 2). To investigate the effect of offsprings own B12 or folate levels on their own birthweight, we performed two-sample MR using the fetal-specific genetic effects from the latest EGG consortium meta-analysis. We used the inverse variance weighted method, and sensitivity analyses to account for pleiotropy, in addition to sensitivity analyses excluding a potentially pleiotropic variant in the FUT2 gene for B12. We did not find evidence for a causal effect of maternal B12 on offspring birthweight, nor evidence for an effect of offspring B12 on their own birthweight using the fetal-specific genetic effect. The results were consistent across the different methods and in sensitivity analyses excluding the FUT2 variant. We found a positive effect of maternal folate on offspring birthweight (0.146 [0.065, 0.227], which corresponds to an increase in birthweight of 71g per 1SD higher folate). We found some evidence for a small inverse effect of fetal folate on their own birthweight (-0.051 [-0.100, -0.003]). In conclusion, our results are consistent with evidence from randomized controlled trials that increased maternal folate levels increase offspring birthweight. We did not find evidence for a causal effect of B12 on offspring birthweight, suggesting previous observational studies may have been due to confounding.

genetics↗

Machine Learning to Predict Osteoporotic Fracture Risk from Genotypes

BackgroundGenomics-based prediction could be useful since genome-wide genotyping costs less than many clinical tests. We tested whether machine learning methods could provide a clinically-relevant genomic prediction of quantitative ultrasound speed of sound (SOS)--a risk factor for osteoporotic fracture.\n\nMethodsWe used 341,449 individuals from UK Biobank with SOS measures to develop genomically-predicted SOS (gSOS) using machine learning algorithms. We selected the optimal algorithm in 5,335 independent individuals and then validated it and its ability to predict incident fracture in an independent test dataset (N = 80,027). Finally, we explored whether genomic pre-screening could complement a UK-based osteoporosis screening strategy, based on the validated tool FRAX.\n\nResultsgSOS explained 4.8-fold more variance in SOS than FRAX clinical risk factors (CRF) alone (r2 = 23% vs. 4.8%). A standard deviation decrease in gSOS, adjusting for the CRF-FRAX score was associated with a higher increased odds of incident major osteoporotic fracture (1,491 cases / 78,536 controls, OR = 1.91 [1.70-2.14], P = 10-28) than that for measured SOS (OR = 1.60 [1.50-1.69], P = 10-52) and femoral neck bone mineral density (147 cases / 4,594 controls, OR = 1.53 [1.27-1.83], P = 10-6). Individuals in the bottom decile of the gSOS distribution had a 3.25-fold increased risk of major osteoporotic fracture (P = 10-18) compared to the top decile. A gSOS-based FRAX score, identified individuals at high risk for incident major osteoporotic fractures better than the CRF-FRAX score (P = 10-14). Introducing a genomic pre-screening step into osteoporosis screening in 4,741 individuals reduced the number of required clinical visits from 2,455 to 1,273 and the number of BMD tests from 1,013 to 473, while only reducing the sensitivity to identify individuals eligible for therapy from 99% to 95%.\n\nInterpretationThe use of genotypes in a machine learning algorithm resulted in a clinically-relevant prediction of SOS and fracture, with potential to impact healthcare resource utilization.\n\nResearch in ContextO_ST_ABSEvidence Before this StudyC_ST_ABSGenome-wide association studies have identified many loci associated with risk of clinically-relevant fracture risk factors, such as SOS. Yet, it is unclear if such information can be leveraged to identify those at risk for disease outcomes, such as osteoporotic fractures. Most previous attempts to predict disease risk from genotypes have used polygenic risk scores, which may not be optimal for genomic-prediction. Despite these obstacles, genomic-prediction could enable screening programs to be more efficient since most people screened in a population are not determined to have a level of risk that would prompt a change in clinical care. Genomic pre-screening could help identify individuals whose risk of disease is low enough that they are unlikely to benefit from screening.\n\nAdded Value of this StudyUsing a large dataset of 426,811 individuals we trained and tested a machine learning algorithm to genomically-predict SOS. This metric, gSOS, had performance characteristics for predicting fracture risk that were similar to measured SOS and femoral neck BMD. Implementing a gSOS-based pre-screening step into the UK-based osteoporosis treatment guidelines reduced the number of individuals who would require screening clinical visits and skeletal testing by approximately 50%, while having little impact on the sensitivity to identify individuals at high risk for osteoporotic fracture.\n\nImplications of all of the Available EvidenceClinically-relevant genomic prediction of heritable traits is feasible using the machine learning algorithm presented here in large sample sizes. Genome-wide genotyping is now less expensive than many clinical tests, needs to be performed once over a lifetime and could risk stratify for multiple heritable traits and diseases years prior to disease onset, providing an opportunity for prevention. The implementation of such algorithms could improve screening efficiency, yet their cost-effectiveness will need to be ascertained in subsequent analyses.

genomics↗

Construction, validation and application of nocturnal pollen transport networks in an agro-ecosystem: a comparison using microscopy and DNA metabarcoding

O_LIMoths are globally relevant as pollinators but nocturnal pollination remains poorly understood. Plant-pollinator interaction networks are traditionally constructed using either flower-visitor observations or pollen-transport detection using microscopy. Recent studies have shown the potential of DNA metabarcoding for detecting and identifying pollen-transport interactions. However, no study has directly compared the realised observations of pollen-transport networks between DNA metabarcoding and conventional light microscopy.\nC_LIO_LIUsing matched samples of nocturnal moths, we construct pollen-transport networks using two methods: light microscopy and DNA metabarcoding. Focussing on the feeding mouthparts of moths, we develop and provide reproducible methods for merging DNA metabarcoding and ecological network analysis to better understand species-interactions.\nC_LIO_LIDNA metabarcoding detected pollen on more individual moths, and detected multiple pollen types on more individuals than microscopy, but the average number of pollen types per individual was unchanged. However, after aggregating individuals of each species, metabarcoding detected more interactions per moth species. Pollen-transport network metrics differed between methods, because of variation in the ability of each to detect multiple pollen types per moth and to separate morphologically-similar or related pollen. We detected unexpected but plausible moth-plant interactions with metabarcoding, revealing new detail about nocturnal pollination systems.\nC_LIO_LIThe nocturnal pollination networks observed using metabarcoding and microscopy were similar, yet distinct, with implications for network ecologists. Comparisons between networks constructed using metabarcoding and traditional methods should therefore be treated with caution. Nevertheless, the potential applications of metabarcoding for studying plant-pollinator interaction networks are encouraging, especially when investigating understudied pollinators such as moths.\nC_LI

ecology↗