bioRxiv Science⌕ Search

bioRxiv · 10.1101/2022.04.11.487885

Using large soybean historical data to study genotype by environment variation and identify mega-environments with the integration of genetic and non-genetic factors

Abstract

1Soybean (Glycine max (L.) Merr.) provides plant-based protein for global food production and is extensively bred to create cultivars with greater productivity in distinct environments. Plant breeders evaluate new soybean genotypes using multi-environment trials (MET). The application of MET assumes that trial locations provide representative environmental conditions that cultivars are likely to encounter when grown by farmers. In addition, MET are important to depict the patterns of genotype by environment interactions (GEI). To evaluate GEI for soybean seed yield and identify mega-environments (ME), a retrospective analysis of 39,006 data points from experimental soybean genotypes evaluated in preliminary and uniform field trials conducted by public plant breeders from 1989-2019 was considered. ME were identified from phenotypic information from the annual trials, geographic, soil, and meteorological records at the trial locations. Results indicate that yield variation was mostly explained by location and location by year interactions. The static portion of the GEI represented 26.30% of the total yield variance. Estimates of variance components derived from linear mixed models demonstrated that the phenotypic variation due to genotype by location interaction effects was greater than genotype by year interaction effects. A trend analysis indicated a two-fold increase in the genotypic variance between 1989-1995 and 1996-2019. Furthermore, the heterogeneous estimates of genotypic, genotype by location, genotype by year, and genotype by location by year variances, were encapsulated by distinct probability distributions. The observed target population of environments can be divided into at least two and at most three ME, thereby suggesting improvements in the response to selection can be achieved when selecting directly for clustered (i.e., regions, ME) versus selecting across regions. Clusters obtained using phenotypic data, latitude, and soil variables plus elevation, were the most effective. In addition, we published the R package SoyURT which contains the data sets used in this work. 2 HighlightsO_LIMega-environments can be identified with phenotypic, geographic, and meteorological data. C_LIO_LIReliable estimates of variances can be obtained with proper analyses of historical data. C_LIO_LIGenotype by location was more important than genotype by year variation for seed yield. C_LIO_LIThe trend in genotype by environment variances was captured in probability distributions. C_LI

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dalsente Krause, M., Olimpio das Gracas Dias, K., Singh, A. K., Beavis, W. D.. 2022-04-11. Using large soybean historical data to study genotype by environment variation and identify mega-environments with the integration of genetic and non-genetic factors. https://doi.org/10.1101/2022.04.11.487885

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

KEEP EXPLORING

Related preprints

Pangenome Discoveries from Clinical Long-Read Genomes in Underrepresented Populations with Neurodevelopmental Disorders

Genetic diagnoses remain elusive for many individuals with neurodevelopmental disorders (NDDs), and the gap is wider in populations poorly represented in genomic reference resources. To demonstrate the equitable advantage of long-read whole genome sequencing (LR-WGS) and pangenomes in terms of clinical utility, we analyzed 211 NDD cases and 107 unaffected relatives from 24 populations, integrating their assemblies, resulting in a total of 1204 haplotypes with the Human Pangenome Reference Consortium Release 2 (HPRC_r2) and the Arab Pangenome Reference (APR) datasets. Clinical interpretation of small variants and structural variants (SVs) revealed pathogenic or likely pathogenic findings in 38.9% of the cases (82/211), and our workflow further detected pathogenic repeat expansions in 3.8% of the cases and runs of homozygosity (ROHs) exceeding 300 Mb in 4.7% of the cases, revealing substantial autozygosity suggestive of strong inbreeding. Beyond these clinical assessments, pangenome analysis revealed 3.9 million population-level novel small variants, 39,782 SVs and an average of 2.17 Mb of novel sequence per individual absent from linear references and global pangenomes. We identified 85.9 kb of case-unique nonreference sequences in exonic segments overlapping with curated NDD gene sets. Graph-based tertiary analysis further identified rare exonic complex homozygous rearrangements in the NDD associated genes for 2.4% of the cases. Together, these findings emphasize how diverse genome assemblies extend variant discovery beyond established linear reference-based clinical interpretation.

genetics↗

Integrated exome-transcriptome analysis of a schizophrenia case with an exceptionally low polygenic risk score

Schizophrenia liability reflects both common polygenic variation and rarer variants of larger effect. We investigated a post-mortem schizophrenia case (SZ07) with a schizophrenia polygenic risk score below the first percentile among ancestry-matched cases, asking whether individual-level genomic and transcriptomic analyses could help identify potentially novel schizophrenia-relevant variants. We used exome analysis with multiple variant-prediction tools to generate a panel of variants and corresponding candidate genes potentially implicated in the pathological process in SZ07. The prioritised variants were then assessed using RNA sequencing of three cortical regions. Of these, only an IZUMO4 splice-acceptor variant showed direct RNA-level support. Beyond variant-specific analyses, we characterised broader transcriptomic abnormalities in the SZ07 brain. Pathway analysis of gene-level expression deviations implicated innate immune processes, calcium signalling, synaptic biology, and axon remodelling. Notably, compared with conventional single-sample biological pathway analysis, the analysis we used showed only a weak association with neuronal specificity, suggesting their reduced sensitivity to the main axis of variation related to cellular composition in bulk brain tissue gene expression data. Although the candidate genes showed no significant pathway-level convergence, the broader transcriptomic profile revealed coherent biological alterations largely compatible with the documented history of cerebrovascular disease in SZ07. These results demonstrate how the integration of exome and transcriptome data at the individual level enables the formulation and constraint of hypotheses regarding patient-specific genetic features and their molecular consequences, while highlighting important limitations related to tissue composition, comorbidity, and the choice of reference cohort.

genetics↗

A genetic screen to identify host factors required for commensal bacterial adherence to the gut epithelia

Bacterial adherence to gut epithelial cells likely involves host genetic components. We isolated a gut commensal bacterium, Lelliottia jeotgali, that can robustly colonize C. elegans through attachment to intestinal epithelial cells. Here, we developed a novel screen in C. elegans to identify host genes required for microbiome bacterial colonization. Using transgenic L. jeotgali strain expressing tdTomato, we conducted forward genetic screens in C. elegans to select for mutants that completely lost colonization. We identified multiple allelic mutations in five different C. elegans genes, termed knockout of Lelliottia adherence (kola) mutants, with a near complete loss of adherence. Each of kola-1-5 is uncharacterized and predicted to encode for a secreted or membrane-bound protein. We also identified gly-5, a GalNAc transferase that initiates O-linked glycosylation. Overall, we describe the first C. elegans screen to identify host factors that control microbiome bacterial colonization in the gut.

genetics↗