ABSTRACT
Complete blood counts (CBCs) measure the abundance of individual immune cells, red blood cells, and related measures such as platelets in circulating blood. These measures can indicate the health status of an animal; thus, baseline circulating levels in a healthy animal may be related to the productive life, resilience, and production efficiency of cattle. The objective of this study is to determine the heritability of CBC traits and identify genomic regions that are associated with CBC measurements in lactating Holstein dairy cattle. The heritability of CBCs was estimated using a Bayes C0 model. The study population consisted of 388 cows with genotypes at roughly 75,000 markers and 16 different CBC phenotypes taken at one to three time points (n = 33, 131, and 224 for 1, 2, and 3 time points, respectively). Heritabilities ranged from 0.00 ± 0.00 (red cell distribution width) to 0.68 ± 0.06 (lymphocytes). A total of 96 different 1-Mb windows were identified that explained more than 1% of the genetic variance for at least one CBC trait, with 10 windows explaining more than 1% of the genetic variance for two or more traits. Multiple genes in the identified regions have functions related to immune response, cell differentiation, anemia, and disease. Positional candidate genes include RAD52 motif-containing protein 1 (RDM1), which is correlated with the degree of immune infiltration of immune cells, and C-X-C motif chemokine ligand 12 (CXCL12), which is critically involved in neutrophil bone marrow storage and release regulation and enhances neutrophil migration. Since animal health directly impacts feed intake, understanding the genetics of CBCs may be useful in identifying more disease-resilient and feed-efficient dairy cattle. Identification of genes responsible for variation in CBCs will also help identify the variability in how dairy cattle defend against illness and injury.
ABSTRACT
Introduction: Pelvic organ prolapse (POP) is one contributor to recent increases in sow mortality that have been observed in some populations and environments, leading to financial losses and welfare concerns. Methods: With inconsistent previous reports, the objective here was to investigate the role of genetics on susceptibility to POP, using data on 30,429 purebred sows, of which 14,186 were genotyped (25K), collected from 2012 to 2022 in two US multiplier farms with a high POP incidence of 7.1% among culled and dead sows and ranging from 2% to 4% of all sows present by parity. Given the low incidence of POP for parities 1 and >6, only data from parities 2 to 6 were retained for analyses. Genetic analyses were conducted both across parities, using cull data (culled for POP versus another reason), and by parity, using farrowing data. (culled for POP versus culled for another reason or not culled). Results and Discussion: Estimates of heritability from univariate logit models on the underlying scale were 0.35 ± 0.02 for the across-parity analysis and ranged from 0.41 ± 0.03 in parity 2 to 0.15 ± 0.07 in parity 6 for the by-parity analyses. Estimates of genetic correlations of POP between parities based on bivariate linear models indicated a similar genetic basis of POP across parities but less similar with increasing distance between parities. Genome wide association analyses revealed six 1 Mb windows that explained more than 1% of the genetic variance in the across-parity data. Most regions were confirmed in several by-parity analyses. Functional analyses of the identified genomic regions showed a potential role of several genes on chromosomes 1, 3, 7, 10, 12, and 14 in susceptibility to POP, including the Estrogen Receptor gene. Gene set enrichment analyses showed that genomic regions that explained more variation for POP were enriched for several terms from custom transcriptome and gene ontology libraries. Conclusion: The influence of genetics on susceptibility to POP in this population and environment was confirmed and several candidate genes and biological processes were identified that can be targeted to better understand and mitigate the incidence of POP.
