SLC39A6/ZIP6 is essential for zinc homeostasis and T-cell development in zebrafish

Biochem Biophys Res Commun. 2019 Apr 16;511(4):896-902. doi: 10.1016/j.bbrc.2019.02.148. Epub 2019 Mar 7.

Abstract

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.

Keywords: T lymphocyte; TALEN; Zebrafish; Zip6.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cation Transport Proteins / genetics*
  • Cation Transport Proteins / metabolism
  • Cells, Cultured
  • Gene Deletion*
  • Gene Expression Regulation, Developmental
  • Homeostasis
  • T-Lymphocytes / cytology
  • T-Lymphocytes / metabolism*
  • Zebrafish / embryology
  • Zebrafish / genetics*
  • Zebrafish / metabolism
  • Zebrafish Proteins / genetics*
  • Zebrafish Proteins / metabolism
  • Zinc / metabolism*

Substances

  • Cation Transport Proteins
  • Zebrafish Proteins
  • slc39a6 protein, zebrafish
  • Zinc