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A complete linkage disequilibrium between the SNP (SNP B) in BCDO2 gene and the yellow skin phenotype in European domestic chicken has been reported. Here, we genotyped the reported SNPs (SNP A, SNP B, and SNP C) of the BCDO2 gene in 183 Chinese Indigenous chickens from 11 breeds/populations, including 57 yellow, 17 white, and 109 black skin chickens. The frequency of all three SNPs were significantly different between yellow and white skin chickens (p<0.01). In black skin chickens, a high frequency of the heterozygous genotype (AG) in SNP A (0.51) and SNP B (0.48) was observed. A total of three haplotypes (AAA, AGA, and GAA) from these three SNPs were obtained. Frequencies of the proposed yellow skin-associated haplotype AGA in yellow skin, white skin, and black skin chickens were 0.81, 0.35, and 0.56, respectively. The results showed that the yellow skin phenotype of the evaluated birds has not been under selection, and that the BCDO2 gene in black skin chickens, evolutionally may undergo a transition phase from yellow to white skin chicken. We concluded that, the SNPs of BCDO2 gene not only can be used to determine whether the chicken was subjected to selection, but may also be used as a marker when selecting for the preferred skin color in chicken breeding programs.

Lipid metabolism dysfunction is closely related to obesity, inflammation, diabetes, lipodystrophy, cardiovascular disease. Along with having a positive effect on energy homeostasis during fasting or prolonged exercise through mitochondrial fatty acid oxidation (FAO), more than two dozen enzymes and transport proteins are involved in the activation and transport of fatty acids into the mitochondrial, providing insights into their critical roles in metabolism. CPT1A has been reported to be expressed ubiquitously in the body and associated with dire consequences affecting fat deposition as the key rate-limiting enzyme of FAO. However, there is a dearth of data on the specific role of CPT1A on adipogenic differentiation and adipocyte lipolysis on chicken. This study assessed CPT1A's function in adipocyte differentiation andadipocyte lipolysis, and the mechanisms were investigated. We found that CPT1A knockdown (KD) promotes the differentiation of chicken preadipocytes into mature adipocytes. CPT1A KD increased PPARγ protein expression level. Expression levels of lipid synthesis-related genes were increased, and lipolysis genes were reduced.Also, CPT1A KD can encourage the formation of lipid droplets. So our results confirmed that knockdown of CPT1A induced the lipid differentiation and inhibited the β-oxidation process to promote the formation of lipid droplets. These findings may deepen our understanding on CPT1A function, especially its regulatory role in adipocyte biology.

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