Melanin is produced from tyrosine catalyzed by tyrosinase undergone a series of catalytic reactions. Age and sunlight exposure are the main causes of inducing the deposition of melanin spots on the human face and neck. In this study, we found that melanin deposition in duck beak skin increased with age. Meanwhile, the melanin deposition in the beak skin of ducks reared under the fully enclosed house was lighter than the ducks feed in the semi-open house system. Our results were consistent with the study by Maddodi et al. in humans, supporting that the melanin spot in the skin is related to age and UV irradiation for both birds and mammals.
In poultry production, it was considered that the deposition of melanin in duck beak skin might be linked to reproductive activities. Previous studies have demonstrated an estrogen receptor in normal human melanocytes[20, 21]. Kim et al. found that estrogen can promote the transport of melanocytes to keratinocytes, resulting in the formation of chloasma. Moreover, estradiol at a definite concentration can also induce deeper skin pigmentation. During the laying period of ducks, the melanin was deposited on the beak surface, and there were individual differences in the amount of melanin deposition. However, a low correlation was observed between melanin deposition in beak skin and reproduction abilities. Therefore, it suggested that the physiological metabolic processes did not cause the melanin deposition in duck beak skin during reproductive activities.
Based on GWAS analysis, three loci associated with melanin amount were identified in the duck genome, and these loci were located on chromosomes 2, 13, and 25, respectively. Our findings implied that melanin deposition in duck beak skin was affected by age and sunlight exposure and genetic factors. Similar results have also been reported in humans[12, 24]. We believed that MITF and POU gene might be the essential candidate genes affecting melanin deposition in duck skin through further fine-mapping works and expression analysis. The MITF protein is considered to be a necessary regulator of melanocyte migration and differentiation. Our findings implied that the melanin synthesis and metabolic pathway played a crucial role in inducing melanin deposition in the skin during age and sunlight exposure. Mutations in any genes related to melanin synthesis and metabolic pathway would affect melanin syntheses, such as MC1R, ENDRB, RAB27A, OA1, PMEL17, MLANA, GPNMB, Melastatin1, Aim1, TYR, TRP-1, TRP-2, and MART-1. Our findings in ducks also served as a reference for human beings to find the causative genes that affect melanin spots under UV irradiation.
Members of the POU transcription factor family can promote transcriptions of many genes related to development and metabolism. This set of gene families shares a typical structure, the POU domain. The name POU derives from the major transcription factors described in the family. POU members have been declared to regulate the transcription of the MITF gene[28, 29]. We found that there are 13 POU gene family members within the duck genome. A total of 44 POU transcription factors were predicted to be distributed within the promoter region of the MITF, and they were POU1F1A, POU1F1B, POU2F1, and POU2F2B. In the candidate region of duck chromosome 25, we found two members of the POU gene family, namely POU2AF1 and POU2F3. The regulatory relationships between POU members and the MITF gene were also supported by the correlation analysis between allele frequencies and phenotypes, which suggested a coordination effect of these two loci on melanin deposition in duck beak skin. Collectively, our data indicated a collaboration effect of MITF and its POU transcription factors on melanin spot deposition on duck beak skin. However, their specific regulatory process needs to be further verified by more molecular biological evidence.
The variations in skin pigmentation are the results of adaptability to various geographical locations[24, 30]. The pivotal function of pigmentation is the protection of the exposed skin against UV radiation. Predictably, genetic variations within the genes involved in the pigmentation process caused phenotypic variations, such as skin pigmentation, hair color, eye color, freckling, and skin sensitivity to sunlight. The ancestor of domestic ducks is the mallard, which is a kind of migratory bird, and the pigmentation variations in the skin are beneficial for adapting to a wide range of environmental conditions. We thus assumed that, after many mutations generated in the MITF and POU during the evolutionary process, the favorable mutations tended to be preserved in duck genomes, to increase the adaptability to different light environments. However, accompanying with age and constant UV irradiation, the asymmetrical distribution of melanocytes caused the formation of melanin spot in duck beak skin. In poultry production, some farmers believed that the melanin spot accumulation in beak skin of ducks is caused by fading of xanthophylls that cover the existing melanin. Nevertheless, our present study has not identified any genes, whose polymorphism related to xanthophylls synthesis were associated with the content of melanin in duck beak skins. The present study, laid new clues for understanding about genetic factors that can affect the melanin spot in the skin, however further investigation required to strengthen this hypothesis.