Search bioRxiv⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2024.06.07.598034

Genotyping-By-Sequencing and DNA array for genomic prediction in soybean oil composition

Prado, M.·Priolli, R. H. G.·Couto, E. G. d. O.·Sabadin, F.·Dias, K. O. d. G.·Pinheiro, J. B.
View original source ↗Export metadata ↓

Abstract

Soybean oil is intended for various purposes, such as cooking oil and biodiesel. The oil composition changes the shelf life, palatability, and how healthy this oil is for the human diet. Genomic selection jointly uses these traits, phenotypes, and markers from one of the available genotyping platforms to increase genetic gain over time. This study aims to evaluate the impact of different genotyping platforms, DNA arrays, and Genotyping-by-Sequencing (GBS) on genomic selection in relation to the composition of fatty acids in soybean oil and total oil content. We used different quality control parameters, such as heterozygote rate, minor allele frequency, and missing data rate in ten combinations, and two prediction models, BayesB and BRR. To compare the impact of the genotyping approaches, we calculated the principal components analysis from the kinship matrices, the SNP density, and the traits prediction accuracies for each approach. Principal component analysis showed that the DNA array explained better the population genetic architecture. On the other hand, prediction accuracies varied between the different genotyping platforms and only GBS was affected under different quality control parameters. Although the DNA array has important and well-studied polymorphisms for soybeans and is stable, it also has ascertainment bias. GBS, although not stable and requires more robust quality control, can discover alleles specific to the population under study. As soybean oil is used for different functions and the fatty acid profiles are different for each objective, the work constitutes a critical study and direction for improving the composition of soybean oil.

Explore related subjects

geneticsPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Prado, M., Priolli, R. H. G., Couto, E. G. d. O., Sabadin, F., Dias, K. O. d. G., Pinheiro, J. B.. 2024-06-09. Genotyping-By-Sequencing and DNA array for genomic prediction in soybean oil composition. https://doi.org/10.1101/2024.06.07.598034

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

KEEP EXPLORING

Related preprints

bioRxiv2026

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↗
bioRxiv2026

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↗
bioRxiv2026

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↗