402V Poster Online - Virtual Posters
Tuesday June 07, 11:00 AM - 3:00 PM

Authors:
Tilman Rönneburg ¹; Yanjun Zan ¹; Christa F Honaker ²; Paul B Siegel ²; Örjan Carlborg ¹

Affiliations:
1) Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden; 2) Department of Animal and Poultry Sciences, Virginia Polytechnic Institute and State University, Blacksburg VA, USA

Keywords:
Complex traits

Genetic analyses of quantitative inherited traits are complex, and studies have often been unable to confidently explain more than a fraction of the heritability of the trait in question. The missing heritability has been attributed to epistasis, or more often to a large number of small, near-zero-effect-size variants. Assuming this, most of the variance will be due to causative variants with minor effects that are difficult to either detect or verify due to power-requirements. In addition, most of the QTL that are large enough to be detected are not single large effect variants, but multiple, smaller QTL in close enough proximity to create a haplotype with an effect large enough to reach the detection threshold. Fine mapping these QTL can be difficult, either due to the small individual effect sizes, haplotype effects, or dependency on the genetic background, thus increasing the requirements for resolution and power. In practice, this leads to a dearth of information on how these broad associations to a phenotype map to the underlying loci. Here, we use low-coverage, whole-genome sequencing data of a large (n>3300), 18-generation advanced intercross line formed from generation 41 of the Virginia body weight lines. The Virginia lines originated from an outbred common stock of White Plymouth Rock chickens and are bi-directionally selected for 8-week body weight. This model system was used to dissect Growth7, a major QTL-region for 8-week body weight and growth-related traits on Chromosome 4. previously, one QTL was mapped and implicated in across-chromosome epistatic interactions using a F₂ cross. Here we mapped four distinct loci in the same region using the advanced intercross line. One locus was an epistatic capacitor, where the two alleles either released or suppressed the effects of the other three loci. In turn, this capacitor was found to be under the epistatic control of another locus on Chromosome 7. This locus was itself previously thought to be part of a nearby large, additive QTL, Growth9. Using the deep intercross population to dissect complex QTL into their components, we not only obtained better estimates and explained variation for the trait, but also gained more insights into the genetic architecture of quantitative trait loci and their phenotypic traits.