Genetics of Ascites Resistance and Tolerance in Chicken: A Random Regression Approach

Abstract

Resistance and tolerance are two complementary mechanisms to reduce the detrimental effects of parasites, pathogens, and production diseases on host performance. Using body weight and ascites data on domesticated chicken Gallus gallus domesticus, we demonstrate the use of random regression animal model and covariance functions to estimate genetic parameters for ascites resistance and tolerance and illustrate the way individual variation in resistance and tolerance induce both genotype re-ranking and changes in variation of host performance along increasing ascites severity. Tolerance to ascites displayed significant genetic variance, with the estimated breeding values of tolerance slope ranging from strongly negative (very sensitive genotype) to weakly negative (less sensitive). Resistance to ascites had heritability of 0.34. Both traits are hence expected to respond to selection. The two complementary defense strategies, tolerance and resistance, were genetically independent. Ascites induced changes to the correlations between ascites resistance and body weight, with the genetic correlations being weak when birds were ascites-free but moderately negative when both healthy and affected birds were present. This likely results because ascites reduces growth, and thus high ascites incidence is genetically related to low adult body weight. Although ascites induced elevated phenotypic and genetic variances in body weight of affected birds, heritability displayed negligible changes across healthy and affected birds. Ascites induced moderate genotype re-ranking in body weight, with the genetic correlation of healthy birds with mildly affected birds being unity but with severely affected birds 0.45. This study demonstrates a novel approach for exploring genetics of defense traits and their impact on genotype-by-environment interactions.

Genetic and phenotypic parameters of carcass and organ traits of broiler chickens

“…Closter et al (2012) reported that the genetic correlations between body weight and the proportion of the heart decreased with a signal change as the age of the chickens increased (0.11± 0.12, -0.09 ± 0.13, and -0.43 ± 0.11 for live weights at 14, 35, and 49 days of age relative to the proportion of the heart, respectively). A similar trend was observed by Kause et al (2012), who found genetic correlation estimates of 0.12 ± 0.12 between live weight at 14 days of age and the proportion of the heart, and -0.33 ± 0.12 between live weight at 49 days of age and the proportion of the heart.…”

Heritable variation in host tolerance and resistance inferred from a wild host–parasite system

“…Studies indicating higher heritability values of resistance (i.e. greater than 20%) have generally been conducted in experimental settings [47,48] whereby non-transmitted factors were controlled for. It is hence likely that our relatively low values of heritability are inherent to the natural settings in which we performed our investigation.…”

Genotype and protein level interaction in growth traits of meat-type quail through reaction norm models

“…Thus, models that are able to accommodate this feature are essentially useful for the modern poultry breeding. The RNM have been generally used to study G×E interaction for disease resistance in other species, such as chicken (Kause et al, 2012), dairy (Calus et al, 2006) and beef (Mota et al, 2016) cattle. However, to our knowledge, studies on trait growth performance under different nutritional levels are still scarce, mainly for meat quail.…”