Summary An F2 population of 239 chickens was obtained by an intercross between Nagoya (NAG), a native Japanese breed with low growth, and White Plymouth Rock (WPR), a Western breed with high growth. Using SNP markers obtained by restriction site‐associated DNA sequencing, genome‐wide QTL analysis was performed and it revealed three QTL for early postnatal growth in the F2 population at genome‐wide 5% significance levels. The most highly significant QTL affecting body weights at 2–4 weeks of age and weight gains at 2–3 and 0–4 weeks was located on GGA4 between 34.0 and 65.6 Mb with LOD scores of 3.9–5.9 and it explained 4.9–9.9% of the total variance of the traits. The analysis provided evidence for significant QTL on GGA2 between 105.6 and 125.2 Mb (LOD = 4.6) and on GGA1 between 51.1 and 61.6 Mb (LOD = 4.0) which had effects on body weight at 3 weeks and body weight gain at 0–1 week respectively. These two genomic regions explained 6.6 and 6.9% of the phenotypic F2 variance of the corresponding traits respectively. The allele derived from WPR at all QTL increased the corresponding traits. Neither sex‐specific nor epistatic QTL was detected. The results showed that the GGA4 QTL affecting multiple traits is a key locus responsible for early growth in our chicken cross, suggesting that this QTL may make a great contribution to genetic improvement of growth performance of the NAG breed with a low growth rate.
Nagoya (NAG), a native Japanese chicken breed, has high quality meat but low meat yield, whereas White Plymouth Rock (WPR), a parental breed of commercial broilers, has rapid growth but high body fat. We previously reported three quantitative trait loci (QTLs) for early postnatal growth in 239 F2 chickens between NAG and WPR breeds. In this study, using the same F2 chickens at 4 weeks of age, we performed genome-wide QTL analysis for breast muscle weight, fat weight and serum and liver levels of biochemical parameters. Two significant QTLs for pectoralis minor and/or major weights were revealed on chromosome 2 between 108 Mb and 127 Mb and chromosome 4 between 10 Mb and 68 Mb. However, no QTL for the other traits was detected. The two QTLs explained 7.0–11.1% of the phenotypic variances, and their alleles derived from WPR increased muscle weights. The chromosome 2 QTL may be a novel locus, whereas the chromosome 4 QTL coincided with a known QTL for meat quality. The findings provide information that is beneficial for genetic improvement of meat yield for the lean NAG breed and, furthermore, provide a better understanding of the genetic basis of chicken muscle development.
A major factor in the propagation of an infectious disease is host genetics. In this study, 180 dairy cows (90 of each breed: Holstein and Montbéliarde) were used. Each breed’s tested dairy cows were divided into two groups of comparable size (45 cows each), mastitis-free and mastitis-affected groups. Each cow’s jugular vein was punctured to obtain blood samples for DNA and RNA extraction. In the examined Holstein and Montbéliarde dairy cows, single nucleotide polymorphisms (SNPs) related with mastitis resistance/susceptibility were found in the RASGRP1, NFkB, CHL1, MARCH3, PDGFD, MAST3, EPS15L1, C1QTNF3, CD46, COX18, NEURL1, PPIE, and PTX3 genes. Chi-square analysis of identified SNPs revealed a significant difference in gene frequency between mastitic and healthy cows. Except for CHL1, mastitic dairy cows of two breeds had considerably higher mRNA levels of the examined genes than did healthy ones. Marker-assisted selection and monitoring of dairy cows’ susceptibility to mastitis may be accomplished through the use of discovered SNPs and changes in the gene expression profile of the studied genes. These findings also point to a possible method for reducing mastitis in dairy cows through selective breeding of animals using genetic markers linked to an animal’s ability to resist infection.
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