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

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 mo...

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Autores principales: Kause, Antti, van Dalen, Sacha, Bovenhuis, Henk
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Genetics Society of America 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362936/
https://www.ncbi.nlm.nih.gov/pubmed/22670223
http://dx.doi.org/10.1534/g3.112.002311
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author Kause, Antti
van Dalen, Sacha
Bovenhuis, Henk
author_facet Kause, Antti
van Dalen, Sacha
Bovenhuis, Henk
author_sort Kause, Antti
collection PubMed
description 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.
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spelling pubmed-33629362012-06-05 Genetics of Ascites Resistance and Tolerance in Chicken: A Random Regression Approach Kause, Antti van Dalen, Sacha Bovenhuis, Henk G3 (Bethesda) Investigations 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. Genetics Society of America 2012-05-01 /pmc/articles/PMC3362936/ /pubmed/22670223 http://dx.doi.org/10.1534/g3.112.002311 Text en Copyright © 2012 Kause et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Unported License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Investigations
Kause, Antti
van Dalen, Sacha
Bovenhuis, Henk
Genetics of Ascites Resistance and Tolerance in Chicken: A Random Regression Approach
title Genetics of Ascites Resistance and Tolerance in Chicken: A Random Regression Approach
title_full Genetics of Ascites Resistance and Tolerance in Chicken: A Random Regression Approach
title_fullStr Genetics of Ascites Resistance and Tolerance in Chicken: A Random Regression Approach
title_full_unstemmed Genetics of Ascites Resistance and Tolerance in Chicken: A Random Regression Approach
title_short Genetics of Ascites Resistance and Tolerance in Chicken: A Random Regression Approach
title_sort genetics of ascites resistance and tolerance in chicken: a random regression approach
topic Investigations
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362936/
https://www.ncbi.nlm.nih.gov/pubmed/22670223
http://dx.doi.org/10.1534/g3.112.002311
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