International Journal of Molecular Evolution and Biodiversity, 2025, Vol.15, No.1, 10-28 http://ecoevopublisher.com/index.php/ijmeb 19 and growth rate. This mutation is more frequent in heavy meat breeds, indicating that humans may have unknowingly selected alleles that affect hunger and improved the growth efficiency of broilers. Similarly, a deletion mutation in IGF2BP1 (IGF2 messenger RNA binding protein 1) was detected in small ornamental chickens, causing these chickens to have limited growth and small body size. Introducing this mutation into ordinary chicken embryos can reproduce the reduced body size phenotype, verifying its functional effect. These examples show that accelerated evolution of growth genes often appears in the form of regulatory element mutations or gene dosage variations and is fixed by artificial selection. In addition to body growth, the reproductive development cycle of domestic chickens is also different from that of wild jungle fowl. Domestic chickens reach sexual maturity at an earlier age, and the annual egg production of hens is much higher than that of jungle fowl. Related hormone and reproductive axis genes also show evolutionary changes after domestication. PRL (prolactin) and VIP (growth hormone release inhibitor) genes are important hormone genes that affect brooding and egg-laying intervals. Studies have found that domestic chicken breeds have variations in the upstream regulatory regions of these genes, which shorten the egg-laying cycle and make it difficult to brood. These variations are almost fixed in high-producing egg-laying chickens, but are rare in jungle fowl. For example, the FSHB (follicle-stimulating hormone beta subunit) gene related to the sexual maturity of roosters has a unique allele combination in some fighting cock breeds. It is speculated that this is a variation that humans have retained in order to breed fighting cocks with strong fighting spirit and late sexual maturity (Guo et al., 2022). Therefore, the functional genes in the growth and reproduction fields have undergone complex selection during the domestication of chickens. Some gene sequences have undergone accelerated evolution (more amino acid changes), while other genes have changed their expression patterns through regulatory evolution. 5.2 Regulatory mutations in feather color, comb shape, and egg-laying traits The color of domestic chicken feathers is mainly determined by the ratio of eumelanin and phenomelanin. The MC1R gene (melanin receptor 1) controls the switch of melanin synthesis, and its active mutation is known to cause the whole body feathers to turn black. Studies have found that in black-feathered black-bone chickens and other breeds, the MC1R gene has amino acid substitutions such as L99P, which stabilizes the receptor configuration in an activated state, continuously stimulates melanin production, and thus darkens the feathers (Huang et al., 2020). In contrast, the MC1R allele carried by wild red junglefowl is less active, allowing the expression of brown-red feathers. Another important gene is ASIP (Agouti signaling protein), which regulates and antagonizes MC1R. The promoter variation of ASIP between different breeds leads to differences in the distribution of melanin in certain parts (such as the neck and wings), resulting in piebald or bicolor feathers (Ouyang et al., 2022). The genetic mechanism that controls white feathers is mainly the blocking of the pigmentation process: some white feather breeds lack the TYR (tyrosinase) gene, causing albinism; more common is recessive white, caused by the variation of the PMEL17 gene (silver gene) that prevents the pigment granules from aggregating into precipitation, and the feathers appear white. At present, through whole genome comparison, the differences between different white feather breeds have also been traced back to their specific gene combinations. For example, the recessive white allele of the White Rock chicken is located at a different locus than that of the White Leghorn chicken, which means that humans have selected the white feather mutation independently and multiple times in different regions. The comb is an important trait of chickens, and its size and shape are determined by cartilage growth. The single comb is the wild type and is produced by the basic developmental program. The pea comb is caused by a mutation in the SOX5 gene: an inversion of about 1.2 Mb is inserted into the first intron of the SOX5 gene on chromosome 1, interfering with its normal expression, causing the comb to change from a single leaf to a three-leaf shape. The rose comb is caused by an inversion on chromosome 7, which includes the sequence of the imaging protein gene MNR2, changes the direction of cartilage differentiation, and makes the comb flat and vine-like. Genetic analysis shows that when the rose comb and pea comb genes interact, new crown types (such as walnut combs) will be produced. These complex phenotypes also have a molecular basis: the inversion of the rose comb and the SOX5 insertion of the pea comb work together to affect the distribution pattern of the blood vessels of the coronoid
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