| Date：2026-6-12 |
| Place：Room 407 |
| Advisor：Pin-Chi Tang |
| Student：Xiu-Min Wu |
| 摘要 |
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Hormones have long been considered as one of the primary factors inducing sexual dimorphism in feather morphology and plumage in mallards (Anas platyrhynchos). Previous studies on the regulation of pigmentation by sex hormones have demonstrated that estradiol (E2), upon binding to its receptors, activates the melanogenesis-related factors (MRFs), thereby promoting melanin production and deposition. After plucking the roosters leg feathers, either E2 or testosterone (T) was implanted. Compared with the untreated controls, E2-treated birds regenerated significantly shorter feathers with more rounded distal ends, resembling the female feather phenotype. These findings demonstrate the reversible regulatory effect of estradiol on feather morphology and suggest that E2 exerts a much greater influence on feather regeneration than T. Gonadectomized male and female mallard ducks exhibit reduced serum E2 concentrations and significantly higher expression levels of MRFs, including microphthalmia-associated transcription factor (MITF) and agouti-signaling protein (ASIP), in feather follicles of the neck region. However, this expression pattern was not significantly correlated with the expression of the classical estrogen receptor alpha (ERα). Recently, a membrane-bound estrogen receptor, G protein-coupled receptor 30 (GPR30), has been reported to participate in skin pigmentation and hair growth, and its selective agonist, G-1, specifically activates GPR30. Therefore, this study aimed to investigate the effects of estrogen and G-1 on the ventral plumage in mallards, and to determine whether sex hormones regulate pigmentation in vitro using cell-based assays. The results showed that ERα mRNA expression in feather follicles was significantly lower in female ducks than in male and castrated male ducks, whereas GPR30 mRNA expression did not differ significantly among groups. Following E2 treatment, the morphology and plumage of regenerated abdominal feathers switched toward a female-like phenotype, while no such changes were observed in the G-1 treatment group, and that the activating effect of G-1 on GPR30 may be limited under the experimental conditions. In addition, in vitro treatment on mouse melanoma cells with 0.8 mM E2 significantly upregulated MITF mRNA expression. In conclusion, these findings demonstrate that exogenous E2 is capable of inducing female phenotypic conversion in castrated male mallards during feather regeneration, and that E2 also regulated the mRNA level of MRFs at the cellular level. Furthermore, GPR30 is unlikely to be the primary estrogen receptor mediating E2-induced feather pigmentation. Therefore, the correlation between estrogen ligands and its receptors, as well as the involvement of the receptor’s downstream in pigmentation pathways, requires further investigation. |
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