Search bioRxiv⌕ Search

bioRxiv · 10.1101/105833

Efficiency of genome-wide association study in random cross populations

Abstract

Genome-wide association studies (GWAS) with plant species have employed inbred lines panels. Our objectives were to present additional quantitative genetics theory for GWAS, evaluate the relative efficiency of GWAS in non-inbred and inbred populations and in an inbred lines panel, and assess factors affecting GWAS. Fifty samples of 400 individuals from populations with linkage disequilibrium were simulated. Individuals were genotyped for 10,000 single nucleotide polymorphisms (SNPs) and phenotyped for traits controlled by 10 quantitative trait loci (QTLs) and 90 minor genes, assuming different degrees of dominance and heritabilities of 40 and 80%. The average SNP density was 0.1 centiMorgan and the QTL heritabilities ranged from 3.2 to 11.8%. To increase the QTL detection power, the additive-dominance model must be fitted for traits controlled by dominance effects but must not be fitted for traits showing no dominance. The power of detection was maximized increasing the sample size to 400 and the false discovery rate (FDR) to 5%. The average power of detection for the low, intermediate, and high heritability QTLs were 9.7, 32.7, and 87.7%, respectively. Under sample size of 400 the observed FDR was equal to or lower than the specified level of significance. The association mapping was highly precise. The analysis of the inbred random cross population provided essentially the same results from the non-inbred population. The inbred lines panel provided the best results concerning the low and intermediate heritability QTL detection power, FDR, and mapping precision. The FDR is mainly affected by population structure, compared to relationship information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Viana, J. M. S., Mundim, G. B., Pereira, H. D., Andrade, A. C. B., Silva, F. F.. 2017-02-03. Efficiency of genome-wide association study in random cross populations. https://doi.org/10.1101/105833

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

KEEP EXPLORING

Related preprints

Mapping, stacking and characterization of a novel resistance haplotype against GpaVvrn-virulent Globodera pallida derived from wild potato relative Solanum brevicaule

Potato production is threatened by pests and pathogens. Among the most harmful are the potato cyst nematodes (PCN), including Globodera pallida. The major control measures are potato cultivars harbouring resistance genes. However, virulent nematode populations are breaking through the most broadly applied resistance genes, and therefore novel resistance genes are required to keep control of G. pallida. In this study we map a resistance locus in wild potato relative Solanum brevicaule to the bottom of chromosome 11 (42.83 - 42.85 Mb) using a k-mer based bulked segregant analysis and name the resistant haplotype GpaXIbrc. The presence of the GpaXIbrc marker in the potato genome significantly increases resistance against a GpaVvrn-virulent G. pallida population (AMPOP01). Furthermore, the GpaXIbrc haplotype was stacked with three other resistance haplotypes: GpaXItar, GpaVvrn, and GpaIXvrn. Stacking of the novel GpaXIbrc haplotype to these other resistance haplotypes resulted in a significant increase in resistance. The largest effect was seen in combinations with 'major' resistance haplotypes GpaVvrn + GpaIXvrn and GpaXItar + GpaXIbrc. To determine whether we are dealing with a novel allele, the resistance mechanism underlying the GpaXIbrc haplotype was described after performing an in vitro bioassay. The resistance mechanism was different from GpaXIspl as described in literature, which is also localized at the bottom of chromosome 11. Therefore, we conclude that we found a novel resistance allele originating from S. brevicaule.

genetics↗

Multiple domains of Mata1 transcription factor contribute to binding site specificity

Among homologous transcription factors with the same function, DNA-binding specificity can diverge. Mat1 is a high mobility group (HMG) box transcription factor in budding yeast whose Saccharomyces cerevisiae and Candida albicans homologs regulate -specific genes but bind distinct cis-regulatory sequences. To identify the protein features underlying this divergence, we generated structure-guided chimeras and measured their activity using species-specific reporters. Replacing any of the four Mat1 regions reduced activation of the S. cerevisiae reporter, while all chimeras retained activity on the C. albicans reporter. Thus, all four regions of Mat - not just the HMG box domain - are important for sequence specificity.

genetics↗

A multi-tissue RNA-seq atlas of adult medaka (Oryzias latipes) under salinity and winter-summer sampling contrasts

Medaka (Oryzias latipes) is a euryhaline and eurythermal teleost widely used in genetics and environmental biology. We generated an RNA-sequencing atlas of 11 adult tissues (brain, eye, gill, heart, intestine, kidney, liver, muscle, spleen, ovary, testis) of the strain d-rR/TOKYO, sampled under two independent environmental contrasts: salinity (freshwater versus seawater) and season (winter versus summer). The freshwater and summer groups, reared indoors and outdoors under long days, provide a third contrast between laboratory and outdoor rearing. Typically, one male and one female were sampled per condition, with ten tissues taken from each individual. Ninety libraries were quantified against the medaka RefSeq transcript set (GCF_053564925.1). The resource comprises gene-level TPM and count matrices, differential expression tables for each tissue and contrast, tissue-specificity indices, human ortholog annotations, sample metadata, and a self-contained interactive browser. Because replication is limited and each condition was sampled on its own date, the differential expression tables are intended for hypothesis generation. The dataset supports studies of gene-expression plasticity and comparisons between medaka and humans.

genetics↗