SLC39A6/ZIP6 is essential for zinc homeostasis and T-cell development in zebrafish
- Zhao, L., Tan, J., Li, D., Jiang, L., Li, T., Yang, Y., Wang, G., Shang, Z., Wang, J., Zhou, J.
- Biochemical and Biophysical Research Communications 511(4): 896-902 (Journal)
- Registered Authors
- T lymphocyte, TALEN, Zebrafish, Zip6
- MeSH Terms
- Cation Transport Proteins/genetics*
- Cation Transport Proteins/metabolism
- Cells, Cultured
- Gene Deletion*
- Gene Expression Regulation, Developmental
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- 30851936 Full text @ Biochem. Biophys. Res. Commun.
Zhao, L., Tan, J., Li, D., Jiang, L., Li, T., Yang, Y., Wang, G., Shang, Z., Wang, J., Zhou, J. (2019) SLC39A6/ZIP6 is essential for zinc homeostasis and T-cell development in zebrafish. Biochemical and Biophysical Research Communications. 511(4):896-902.
Zinc (Zn) is an essential trace element that modulate innate and acquired immune responses, and its deficiency triggers lymphopenia. However, the precise mechanisms underlying zinc-mediated lymphocyte maintenance have not been well clarified. Here, we have successfully generated a zip6-null mutant zebrafish line using TALENs. The Zip6-null mutant zebrafish developed normally during gastrulation. Loss of zip6 in zebrafish resulted in significant T lymphocyte reduction and a decrease in intracellular Zn levels. And the zip6 deficiency increases caspase-related cell apoptosis in both zebrafish cells and human T cells. Our results suggest that ZIP6 plays a critical part in T cell development, and enhance our understanding of Zn homeostasis and immune system maintenance.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes