Background: The objective of any valid breeding program is to increase the suitability of a breed for its future purposes. The approach most often followed in animal breeding for optimizing breeding goals assumes that the sole desire of the owners is profit maximization. As this assumption is often violated, a generalized approach is needed that does not rely on this assumption.
Results: The generalized approach is based on the niche concept. The niche of a breed is a set of environments in which a small population of the breed would have a positive population growth rate. Its growth rate depends on demand from prospective consumers and supply from producers. The approach involves defining the niche that is envisaged for the breed and identifying the trait optima that maximize the breed's adaptation to its envisaged niche within the set of permissible breeding goals. The set of permissible breeding goals is the set of all potential breeding goals that are compatible with animal welfare and could be reached within the planning horizon of the breeding program. In general, the breed's adaptation depends on the satisfaction of the producers with the animals and on the satisfaction of the consumers with the products produced by the animals. When consumers buy live animals, then the breed needs to adapt to both the environments provided by the producers, and the environments provided by the consumers. The profit function is replaced by a more general adaptedness function that measures the breed's adaptation to its envisaged niche.
Conclusions: The proposed approach coincides with the traditional approach if the producers have the sole desire to maximize their income, and if consumer preferences are well reflected by the product prices. If these assumptions are not met, then the traditional approach to breeding goal optimization is unlikely to result in a valid breeding goal. Using the example of companion breeds, this paper shows that the proposed approach has the potential to fill the gap.
Background: Host resilience (HR) to parasites can affect the performance of animals. Therefore, the aim of this study was to present a detailed investigation of the genetic mechanisms of HR to ticks (TICK), gastrointestinal nematodes (GIN), and Eimeria spp. (EIM) in Nellore cattle that were raised under natural infestation and a prophylactic parasite control strategy. In our study, HR was defined as the slope coefficient of body weight (BW) when TICK, GIN, and EIM burdens were used as environmental gradients in random regression models. In total, 1712 animals were evaluated at five measurement events (ME) at an average age of 331, 385, 443, 498, and 555 days, which generated 7307 body weight (BW) records. Of the 1712 animals, 1075 genotyped animals were used in genome-wide association studies to identify genomic regions associated with HR.
Results: Posterior means of the heritability estimates for BW ranged from 0.09 to 0.54 across parasites and ME. The single nucleotide polymorphism (SNP)-derived heritability for BW at each ME ranged from a low (0.09 at ME.331) to a moderate value (0.23 at ME.555). Those estimates show that genetic progress can be achieved for BW through selection. Both genetic and genomic associations between BW and HR to TICK, GIN, and EIM confirmed that parasite infestation impacted the performance of animals. Selection for BW under an environment with a controlled parasite burden is an alternative to improve both, BW and HR. There was no impact of age of measurement on the estimates of genetic variance for HR. Five quantitative trait loci (QTL) were associated with HR to EIM but none with HR to TICK and to GIN. These QTL contain genes that were previously shown to be associated with the production of antibody modulators and chemokines that are released in the intestinal epithelium.
Conclusions: Selection for BW under natural infestation and controlled parasite burden, via prophylactic parasite control, contributes to the identification of animals that are resilient to nematodes and Eimeria ssp. Although we verified that sufficient genetic variation existed for HR, we did not find any genes associated with mechanisms that could justify the expression of HR to TICK and GIN.