Search bioRxiv⌕ Search

bioRxiv · 10.1101/2024.11.22.624688

Estimating hierarchical F-statistics from Pool-Seq data

Abstract

Introduced over seventy years ago, F -statistics have been and remain central to population and evolutionary genetics. Among them, FST is one of the most commonly used descriptive statistics in empirical studies, notably to characterize the structure of genetic polymorphisms within and between populations, to shed light on the evolutionary history of populations, or to identify marker loci under differential selection for adaptive traits. However, the use of FST in simplified population models can overlook important hierarchical structures, such as geographic or temporal subdivisions, potentially leading to misleading interpretations and increasing false positives in genome scans for adaptive differentiation. Hierarchical F -statistics have been introduced to account for multiple predefined levels of population structure. Several estimators have also been proposed, including robust ones implemented in the popular R package hierfstat. Nevertheless, these were primarily designed for individual genotyping data and can be computationally intensive for large genomic datasets. In this study, we extend previous work by developing unbiased method-of-moments estimators for hierarchical F -statistics tailored for Pool-Seq data, a cost-effective alternative to individual genome sequencing. These Pool-Seq estimators have been developed in an anova framework, using definitions based on identity-in-state probabilities. The new estimators have been implemented in an updated version of the R package poolfstat, together with estimators for sample allele count data derived from individual genotyping data. We validate and compare the performance of these estimators through extensive simulations under a hierarchical island model. Finally, we apply these estimators to real Pool-Seq data from Drosophila melanogaster populations, demonstrating their usefulness in revealing population structure and identifying loci with high differentiation within or between groups of subpopulations and associated with spatial or temporal genetic variation.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Gautier, M., Coronado-Zamora, M., Vitalis, R.. 2024-11-22. Estimating hierarchical F-statistics from Pool-Seq data. https://doi.org/10.1101/2024.11.22.624688

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

A largely shared genetic architecture underlies Saccharomyces cerevisiae persistence across different mouse host genotypes

The extent to which interactions between microbial and host genotypes shape opportunistic pathogen persistence within hosts is an important open question. To assess the contribution of these interactions to persistence, we used Saccharomyces cerevisiae , a genetically tractable model for studying opportunistic fungal persistence in mammalian hosts. A pooled panel of barcoded haploid segregants from a cross between a laboratory strain and a clinical isolate, together with both parents, was introduced intravenously into seven genetically diverse mouse strains. We measured the relative persistence of segregants in mouse brains and livers using barcode sequencing. Persistence showed transgressive segregation in both organs. On average across the two organs, yeast genotype explained 45.2% of the variance in segregant persistence, whereas yeast genotype-by-host genotype interactions explained only 2.9%. Linkage mapping showed that loci detected in more host genotypes generally explained more phenotypic variance than those detected in fewer host genotypes. At some loci, genetic variation correlated with increased yeast persistence across multiple organs (general loci) while at others increased persistence in one organ came at the cost of decreased persistence in another (antagonistic loci). General loci contributed disproportionately to brain persistence, whereas liver persistence reflected contributions from both classes. The clinical parent showed greater persistence than the laboratory parent in every host-organ combination, and the additive effects of detected loci predicted the direction of this advantage. Overall, this work shows that in this system, relative microbial persistence is polygenic, with a strong additive component and only a very small contribution from microbial genotype-by-host genotype interactions.

genetics↗

Host control and regulation of human anellovirus persistence

Anelloviruses are the most abundant and diverse eukaryotic viruses known to infect humans and can persist throughout our lifetimes. Despite their ubiquity, the host factors governing their physiologic distribution and abundance remain poorly understood. Here, we construct a viral pangenome of 2,023 strains to quantify anellovirus DNA in >1.1 million participants spanning three genetic biobanks. Genome-wide association studies identify 121 loci linked to viral persistence, predominantly via immune regulation by NF-kB signaling. Further, we associate variable anellovirus detection with conditions characterized by immune dysfunction, including lymphoid malignancies. By screening 3.2 petabases of human single-cell sequencing data, we identify myeloid progenitors in the bone marrow as a prominent site of anellovirus transcription in vivo. Finally, Perturb-seq of anellovirus proteins reveals that anellovirus ORF2, particularly from Alphatorquevirus, attenuates TNF-a-induced NF-kB signaling, connecting host genetic variation, cellular context, and viral immunomodulation to characterize the persistence of the eukaryotic human virome's most abundant component.

genetics↗

Regulation of sociality and neuronal development by the translation initiation factor eIF4H1 in Drosophila

Most animal species exhibit some level of sociality. However, whether sociality-related traits evolved independently, or are instead derived from common core mechanisms, remains controversial. Nevertheless, an emerging theoretical framework stipulates that key aspects of how animals interact with their social environments may be regulated by a phylogenetically conserved genetic toolkit. Therefore, we hypothesized that mutations that lead to social deficits in specific human disorders may implicate genes that play conserved roles in the regulation of core social traits across Animalia. Specifically, here we focus on genes associated with Williams syndrome (WS), a rare human multi-system disorder characterized in part by hypersocial cognitive traits. WS is caused by a hemizygous chromosomal microdeletion of 25-28 protein-coding genes. Consequently, it has been hypothesized that haploinsufficiency in at least one of these genes plays an important role in the development and/or function of social neural circuits in humans. Because the Drosophila genome encodes orthologs of 17 of the 28 genes deleted in WS, we reasoned that at least some of them may serve a conserved role in the regulation of social traits across flies and humans, as predicted by the genetic toolkit framework. Using a neuron-specific RNAi knockdown screen, we identified eIF4H1, an ortholog of a highly conserved subunit of the eukaryotic translation initiation complex eIF4F, as a candidate gene for neuronal regulation of sociality in the fly. We show that eIF4H1 expression is predominantly neuronal in the adult fly brain, and that its action plays a differential role in the organization of specific dopaminergic neuron subtypes that are associated with sociality and cognitive functions. These results indicate that eIF4H1 may serve a conserved function in regulating the development of the neuronal circuits that regulate social behaviors, thus supporting the idea of a conserved sociality genetic toolkit.

genetics↗