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Date of Award
Spring 4-16-2018
Degree Type
Thesis
Degree Name
Bachelor of Science
Department
Biomedical Sciences
First Advisor
Lidia Kos
Abstract
Melanocortin Receptor 1 (Mc1r) signaling is essential for proper pigment production. In its absence, mice are unable to produce eumelanin and display a yellow coat color as seen in lethal yellow mice (A y ). Previous members of my lab have shown that Endothelin Receptor b (EdnrB) signaling can compensate for the lack of Mc1r in pigment production by crossing A y mice with hyperpigmented inducible transgenic mice that over-express the EndrB ligand endothelin 3 in the skin (K5tTA-Edn3). The goal of this study was to determine the mechanism of action for Edn3 signaling in rescuing the coat color phenotype of A y mice. To determine if the darker coat color of K5tTA-Edn3 mice resulted from an increase in the number of follicular melanocytes, I performed immunofluorescence with Tyrp1 antibody. The numbers of follicular melanocytes in transgenic and control mice were not significantly different. I used qRT-PCR to evaluate if the darkened coat color produced by Edn3 overexpression is a result of melanogenic gene regulation in follicular melanocytes. There was at least a two-fold increase in the expression of Mitf, Tyrosinase and Trp1 in the hair follicles of Ay ; K5-Edn3 mice when compared with those of control animals. Additionally, transgenic animals upregulated slc7a11, implying an increased co-production of pheomelanin and eumelanin in these mice. Together these results show that Edn3 should be considered as an important player in melanin production and regulation.
Recommended Citation
Durango, Alexander, "Mechanism of Endothelin3 Regulation on Murine Coat Color" (2018). Department of Biological Sciences - Undergraduate Honors Theses. 81.
https://digitalcommons.fiu.edu/bio_honors/81
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