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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., (© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society of Animal Science.)

Increased milk production due to high litter size, coupled with low feed intake, results in excessive mobilization of sow body reserves during lactation, which can have detrimental effects on future reproductive performance. A possibility to prevent this is to improve sow lactation performance genetically, along with other traits of interest. The aim of this study was to estimate breed-specific genetic parameters (by parity, between parities, and across parities) for traits associated with lactation and reproduction in Yorkshire and Landrace sows. Performance data were available for 2,107 sows with 1 to 3 parities (3,424 farrowings total). Sow back fat, loin depth and BW at farrowing, sow feed intake (SFI), and body weight loss (BWL) during lactation showed moderate heritabilities (0.21 to 0.37) in both breeds, whereas back fat loss (BFL), loin depth loss (LDL), and litter weight gain (LWG) showed low heritabilities (0.12 to 0.18). Among the efficiency traits, sow lactation efficiency showed extremely low heritability (near zero) in Yorkshire sows but a slightly higher (0.05) estimate in Landrace sows, whereas sow residual feed intake (SRFI) and energy balance traits showed moderate heritabilities in both breeds. Genetic correlations indicated that SFI during lactation had strong negative genetic correlations with body resource mobilization traits (BWL, BFL, and LDL; -0.35 to -0.70), and tissue mobilization traits in turn had strong positive genetic correlations with LWG (+0.24 to +0.54; < 0.05). However, SFI did not have a significant genetic correlation with LWG. These genetic correlations suggest that SFI during lactation is predominantly used for reducing sow body tissue losses, rather than for milk production. Estimates of genetic correlations for the same trait measured in parities 1 and 2 ranged from 0.64 to 0.98, which suggests that first and later parities should be treated as genetically different for some traits. Genetic correlations estimated between traits in parities 1 and 2 indicated that BWF and BWL measured in parity 1 can be used as indicator traits for SFI and SRFI measured in parities 1 and 2. In conclusion, traits associated with lactation in sows have a sizable genetic component and show potential for genetic improvement.

Lactation is an economically and biologically important phase in the life cycle of sows. Short generation intervals in nucleus herds and low heritability of traits associated with lactation along with challenges associated with collecting accurate lactation performance phenotypes emphasize the importance of using genomic tools to examine the underlying genetics of these traits. We report the first genomewide association study (GWAS) on traits associated with lactation and efficiency in 2 lines of Yorkshire pigs that were divergently selected for residual feed intake during grow-finish phase. A total of 862 farrowing records from 2 parities were analyzed using a Bayesian whole genome variable selection model (Bayes B) to locate 1-Mb regions that were most strongly associated with each trait. The GWAS was conducted separately for parity 1 and 2 records. Marker-based heritabilities ranged from 0.03 to 0.39 for parity 1 traits and from 0.06 to 0.40 for parity 2 traits. For all traits studied, around 90% of genetic variance came from a large number of genomic regions with small effects, whereas genomic regions with large effects were found to be different for the same trait measured in parity 1 and 2. The highest percentage of genetic variance explained by a 1-Mb window for each trait ranged from 0.4% for feed intake during lactation to 4.2% for back fat measured at farrowing in parity 1 sows and from 0.2% for lactation feed intake to 5.4% for protein mass loss during lactation in parity 2 sows. A total of thirteen 1-Mb nonoverlapping windows were found to explain more than 1.5% of genetic variance for either a single trait or across multiple traits. These 1-Mb windows were on chromosomes 2, 3, 6, 7, 8, 11, 14, 15, 17, and 18. The major positional candidate genes within 1 Mb upstream and downstream of these windows were , (SSC2), (SSC6) (SSC7), (SSC8), (SSC11), (SSC14), (SSC17). Further validation studies on larger populations are required to validate these findings and to improve our understanding of the biology and complex genetic architecture of traits associated with sow lactation performance.

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., (Copyright © 2015 by The American Association of Immunologists, Inc.)