Variance component estimates for growth traits in beef cattle using selected variants from imputed low-pass sequence data

Abstract

Abstract A beef cattle population (n = 2,343) was used to assess the impact of variants identified from the imputed low-pass sequence (LPS) on the estimation of variance components and genetic parameters of birth weight (BWT) and post-weaning gain (PWG). Variants were selected based on functional impact and were partitioned into four groups (low, modifier, moderate, high) based on predicted functional impact and re-partitioned based on the consequence of mutation, such as missense and untranslated region variants, into six groups (G1-G6). Each subset was used to construct a genomic relationship matrix (GRM) for univariate animal models. Multiple analyses were conducted to compare the proportion of additive genetic variation explained by the different subsets individually and collectively, and these estimates were benchmarked against all LPS variants in a single GRM and array (e.g., GeneSeek Genomic Profiler 100K) genotypes. When all variants were included in a single GRM, heritability estimates for BWT and PWG were 0.43 ± 0.05 and 0.38 ± 0.05, respectively. Heritability estimates for BWT ranged from 0.10 to 0.42 dependent on which variant subsets were included. Similarly, estimates for PWG ranged from 0.05 to 0.38. Results showed that variants in the subsets modifier and G1 (untranslated region) yielded the highest heritability estimates and were similar to the inclusion of all variants, while estimates from GRM containing only variants in the categories High, G4 (non-coding transcript exon), and G6 (start and stop loss/gain) were the lowest. All variants combined provided similar heritability estimates to chip genotypes and provided minimal to no additional information when combined with chip data. This suggests that the chip single nucleotide polymorphisms and the variants from LPS predicted to be less consequential are in relatively high linkage disequilibrium with the underlying causal variants as a whole and sufficiently spread throughout the genome to capture larger proportions of additive genetic variation.