Samuel Restrepo

Document Type

Limited Access




Neural crest cells are a population of undifferentiated, multipotent cells that differentiate into a vast array of adult cell types. As part of their development, they undergo an epithelial-to-mesenchymal transition (EMT) at the dorsal neural tube to migrate throughout the embryo. An unregulated EMT occurs in cancers such as malignant melanoma, where neural crest-derived melanocytes invade other tissues of the adult body. In the zebrafish, Danio rerio, the neural crest generates three pigment cell types: black melanocytes, iridescent iridophores, and yellow xanthophores. The changes in gene expression that regulate migration, specification, and differentiation of neural crest cells into fully mature pigment cells are still not fully elucidated. Previous studies suggest that some iridophores and melanocytes share a precursor and that an unknown transcription factor is required to promote iridophore fate. Recent work showed that alx4a and alx4b are highly expressed in iridophores and not in melanocytes. I hypothesized that alx4a and/or alx4b act to inhibit melanocyte fate and promote iridophore fate. To test the roles of alx4a and alx4b in pigment cell fate, we designed and constructed a series of expression clones. These expression clones were injected into wild-type (WT) zebrafish embryos at the 1-cell stage, and embryos were examined for fluorescent reporters and alterations in pigment cell development. Identifying and understanding the genes required for iridophore fate specification and melanocyte repression may provide valuable insight into neural crest-derived cancers such as malignant melanoma.


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