Purebred-crossbred genetic parameters for reproductive traits in swine.

For swine breeding programs, testing and selection programs are usually within purebred (PB) populations located in nucleus units that are generally managed differently and tend to have a higher health level than the commercial herds in which the crossbred (CB) descendants of these nucleus animals are expected to perform. This approach assumes that PB animals selected in the nucleus herd will have CB progeny that have superior performance at the commercial level. There is clear evidence that this may not be the case for all traits of economic importance and, thus, including data collected at the commercial herd level may increase the accuracy of selection for commercial CB performance at the nucleus level. The goal for this study was to estimate genetic parameters for five maternal reproductive traits between two PB maternal nucleus populations (Landrace and Yorkshire) and their CB offspring: Total Number Born (TNB), Number Born Alive (NBA), Number Born Alive > 1 kg (NBA > 1 kg), Total Number Weaned (TNW), and Litter Weight at Weaning (LWW). Estimates were based on single-step GBLUP by analyzing any two combinations of a PB and the CB population, and by analyzing all three populations jointly. The genomic relationship matrix between the three populations was generated by using within-population allele frequencies for relationships within a population, and across-population allele frequencies for relationships of the CB with the PB animals. Utilization of metafounders for the two PB populations had no effect on parameter estimates, so the two PB populations were assumed to be genetically unrelated. Joint analysis of two (one PB plus CB) vs. three (both PB and CB) populations did not impact estimates of heritability, additive genetic variance, and genetic correlations. Heritabilities were generally similar between the PB and CB populations, except for LWW and TNW, for which PB populations had about four times larger estimates than CB. Purebred-crossbred genetic correlations (rpc) were larger for Landrace than for Yorkshire, except for NBA > 1 kg. These estimates of rpc indicate that there is potential to improve selection of PB animals for CB performance by including CB information for all traits in the Yorkshire population, but that noticeable additional gains may only occur for NBA > 1 kg and TNW in the Landrace population.

Genetic parameters and purebred-crossbred genetic correlations for growth, meat quality, and carcass traits in pigs.

Growth, meat quality, and carcass traits are of economic importance in swine breeding. Understanding their genetic basis in purebred (PB) and commercial crossbred (CB) pigs is necessary for a successful breeding program because, although the breeding goal is to improve CB performance, phenotype collection and selection are usually carried out in PB populations housed in biosecure nucleus herds. Thus, the selection is indirect, and the accuracy of selection depends on the genetic correlation between PB and CB performance (rpc). The objectives of this study were to 1) estimate genetic parameters for growth, meat quality, and carcass traits in a PB sire line and related commercial CB pigs and 2) estimate the corresponding genetic correlations between purebred and crossbred performance (rpc). Both objectives were investigated by using pedigree information only (PBLUP) and by combining pedigree and genomic information in a single-step genomic BLUP (ssGBLUP) procedure. Growth rate showed moderate estimates of heritability for both PB and CB based on PBLUP, while estimates were higher in CB based on ssGBLUP. Heritability estimates for meat quality traits were diverse and slightly different based on PB and CB data with both methods. Carcass traits had higher heritability estimates based on PB compared with CB data based on PBLUP and slightly higher estimates for CB data based on ssGBLUP. A wide range of estimates of genetic correlations were obtained among traits within the PB and CB data. In the PB population, estimates of heritabilities and genetic correlations were similar based on PBLUP and ssGBLUP for all traits, while based on the CB data, ssGBLUP resulted in different estimates of genetic parameters with lower SEs. With some exceptions, estimates of rpc were moderate to high. The SE on the rpc estimates was generally large when based on PBLUP due to limited sample size, especially for CBs. In contrast, estimates of rpc based on ssGBLUP were not only more precise but also more consistent among pairs of traits, considering their genetic correlations within the PB and CB data. The wide range of estimates of rpc (less than 0.70 for 7 out of 13 traits) indicates that the use of CB phenotypes recorded on commercial farms, along with genomic information, for selection in the PB population has potential to increase the genetic progress of CB performance.

Not All SCID Pigs Are Created Equally: Two Independent Mutations in the Artemis Gene Cause SCID in Pigs.

Mutations in >30 genes are known to result in impairment of the adaptive immune system, causing a group of disorders collectively known as SCID. SCID disorders are split into groups based on their presence and/or functionality of B, T, and NK cells. Piglets from a line of Yorkshire pigs at Iowa State University were shown to be affected by T(-)B(-)NK(+) SCID, representing, to our knowledge, the first example of naturally occurring SCID in pigs. In this study, we present evidence for two spontaneous mutations as the molecular basis for this SCID phenotype. Flow cytometry analysis of thymocytes showed an increased frequency of immature T cells in SCID pigs. Fibroblasts from these pigs were more sensitive to ionizing radiation than non-SCID piglets, eliminating the RAG1 and RAG2 genes. Genetic and molecular analyses showed that two mutations were present in the Artemis gene, which in the homozygous or compound heterozygous state cause the immunodeficient phenotype. Rescue of SCID fibroblast radiosensitivity by human Artemis protein demonstrated that the identified Artemis mutations are the direct cause of this cellular phenotype. The work presented in the present study reveals two mutations in the Artemis gene that cause T(-)B(-)NK(+) SCID in pigs. The SCID pig can be an important biomedical model, but these mutations would be undesirable in commercial pig populations. The identified mutations and associated genetic tests can be used to address both of these issues.