Abstract
High environmental temperature is a serious stress affecting economic and biological efficiency of poultry production in tropical and subtropical countries that is expected to become more prominent with global climate change. Iowa experienced 3 acute heat waves of 11, 3, and 4 d of heat index above 38°C in the summer of 2012, which led to production losses and increased bird mortality. For the current study, the proportion of daughters that died from heat stress during this period was calculated for 118 sire families of an elite White Leghorn layer line. The number of daughters per sire ranged from 25 to 111 and averaged 68. Average mortality due to heat stress was 8.2%, ranging from 0 to 24.6%. All sires were genotyped using a 600K Affymetrix chip. After stringent quality filtering (clustering quality, parentage, missing genotypes, MAF) 113,344 SNPs were retained for the analysis. Method BayesB with π equal to 0.999, for the number of markers fitted not to exceed the number of observations, was applied. Markers explained 8% of the phenotypic variance. One 1-Mb window on chromosome 5 explained 1.2% of genetic variance. When the number of daughters was fitted as a weight in the analysis, the proportion of variance explained by markers dropped to 1%, but 9 1-Mb windows explained more than 1% of genetic variance on chromosomes 1, 3, 5 (the same top window as in the unweighted analysis), 9, 17, and 18. Although the support of the genomic regions associated with heat stress resistance identified in this study was not very strong, they overlapped with previously reported quantitative trait loci regions for immune response and physiological traits in chickens and contained genes that have been associated with response to heat stress in other studies. Further research is needed to validate the results.
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