Daniel C. Ciobanu
,
University of Nebraska - Lincoln, Lincoln, NE
Emily Tosky
,
University of Nebraska - Lincoln, Lincoln, NE
Sean Olson
,
University of Nebraska - Lincoln, Lincoln, NE
Melanie Trenhaile
,
University of Nebraska - Lincoln, Lincoln, NE
Clay A Lents
,
USDA, ARS, USMARC, Clay Center, NE
Timothy P.L. Smith
,
USDA, ARS, USMARC, Clay Center, NE
Dan Nonneman
,
USDA, ARS, USMARC, Clay Center, NE
Gary A. Rohrer
,
USDA, ARS, USMARC, Clay Center, NE
Jason Chin
,
Pacific Biosciences, Menlo Park, CA
Phillip S. Miller
,
University of Nebraska - Lincoln, Lincoln, NE
Thomas Burkey
,
University of Nebraska - Lincoln, Lincoln, NE
Matt L. Spangler
,
University of Nebraska - Lincoln, Lincoln, NE
Jean-Jack Riethoven
,
University of Nebraska - Lincoln, Lincoln, NE
Graham S Plastow
,
University of Alberta, Edmonton, AB, Canada
Stephen D. Kachman
,
University of Nebraska - Lincoln, Lincoln, NE
Commercial and experimental genetic resources were established and investigated for a range of reproductive and disease susceptibility phenotypes. These efforts were complemented with RNA and whole genome sequencing and new assemblies of the swine genome. Data generation efforts were accompanied by the development of novel statistical approaches, integrating haplotype analysis and interval mapping in a Bayesian framework to explore genetic variation of multiple traits.
Specifically, sources of variation in expression of puberty and fertility were investigated by RNAseq of hypothalamic arcuate nucleus, various GWAS approaches, and genome sequencing of sires with early and late puberty daughters. Various subsets of SNPs from major 1-Mb windows that explained the largest proportions of variation in training populations were evaluated to assess the potential of reduced sets of SNP to explain phenotypic variation for age at puberty. Relative to disease, a major QTL for PCV2 viremia previously reported was fine mapped on a novel 29 Mb scaffold based on long sequencing reads while gene prediction and annotation provided potential candidates responsible for the observed variation. In addition, new PCV2 challenges targeting pigs of different QTL genotypes in experimentally infected and vaccinated animals confirmed previous results and provided evidence of the host genetic role in viral replication.
