PUBLICATION

Zinc transporter Slc30a1 regulates melanocyte development by interacting with mt2 in zebrafish

Authors
Xia, Z., Yang, X., Bi, X., Tong, X., Min, J., Wang, F.
ID
ZDB-PUB-220907-16
Date
2022
Source
European journal of cell biology   101: 151272 (Journal)
Registered Authors
Min, Junxia, Wang, Fudi, Xia, Zhidan
Keywords
Melanocyte, Slc30a1, Zebrafish, Zinc homeostasis, mt2
MeSH Terms
  • Animals
  • Melanocytes/metabolism
  • Melanoma*/genetics
  • Melanoma*/metabolism
  • Zebrafish*/genetics
  • Zebrafish*/metabolism
  • Zinc/metabolism
PubMed
36063588 Full text @ Eur. J. Cell Biol.
Abstract
The essential trace element zinc is involved in multiple biological processes including development and metabolism, while its role in melanocyte formation is still unclear. Slc30a1a and Slc30a1b are zinc exporters in zebrafish. Here, we found that melanocytes were increased in slc30a1a and slc30a1b double mutant zebrafish. SMART-seq data revealed that genes involved in the melanoma pathway and the gene mt2, which encodes zinc-binding protein, were significantly upregulated in the mutants. In addition, the expression of mt2 was specifically increased in mutant melanocytes, as detected by in situ hybridization, suggesting an essential role of this gene in the tissue. Mechanistically, we demonstrated that elevated zinc levels resulting from Slc30a1 deficiency promoted melanocyte proliferation and that mt2 played a protective role in the process of Slc30a1/zinc-mediated melanocyte hyperplasia. This study uncovered the critical function of Slc30a1-mediated zinc homeostasis in melanocyte development and suggests that accumulated zinc in melanocytes would be a risk for inducing melanoma and that mt2 is a potential target for controlling diseases related to abnormal melanocyte development.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping