Effect of a single-nucleotide polymorphism in the Cholecystokinin Type A Receptor gene on growth traits in the Hinai-dori chicken breed
2013
Rikimaru, K. ((Akita Prefectural Livestock Experiment Station, Daisen (Japan)), (Tohoku University, Sendai (Japan). Graduate School of Agricultural Science)) | Takeda, H. | Uemoto, Y. | Komatsu, M. | Takahashi, D. | Suzuki, K. | Takahashi, H.
We have previously reported the association between chicken cholecystokinin type A receptor gene (CCKAR) haplotypes and growth traits in an F2 resource population produced by crossing low- and high-growth lines of the Hinai-dori breed. The high-growth line was developed from a low-growth founder from the Preservation Society of the Hinai-dori breed by long-term selection for growth performance at the Akita Prefectural Livestock Experiment Station. In the present study, we determined the effect of a single-nucleotide polymorphism (SNP, AB604331: g.420 C>A in the 5' -untranslated region of CCKAR on the growth traits of the F2 population. A mismatch amplification mutation polymerase chain reaction assay was developed to distinguish between the 3 genotypes (A/A, A/C, and C/C) in the F2 population, and effect of the SNP on growth traits was estimated. The data showed that body weight at 10 and 14 weeks of age, and average daily gain between 4 and 10 weeks, 10 and 14 weeks, and 0 and 14 weeks of age in individuals with the A allele was superior to that in those with the C allele. The electrophoretic mobility shift assay was performed to clarify the contribution of the g. 420 C>A SNP in the predicted YY1 binding site. As a result, the YY1 protein showed a stronger binding affinity for g.420 A probe, suggesting the possibility that the SNP affects transcriptional efficiency of the CCKAR. The A allele frequencies in the high- and low-growth lines maintained in fiscal year 2010 were 0.889 and 0.124, respectively. The difference in the allele frequencies of these lines is thought to be caused by long-term selection for growth performance since the probability was too significantly (P<0.01) low to be caused by random genetic drift.
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