ZFIN ID: ZDB-PUB-120823-9
Slc39a7/zip7 Plays a Critical Role in Development and Zinc Homeostasis in Zebrafish
Yan, G., Zhang, Y., Yu, J., Yu, Y., Zhang, F., Zhang, Z., Wu, A., Yan, X., Zhou, Y., and Wang, F.
Date: 2012
Source: PLoS One   7(8): e42939 (Journal)
Registered Authors: Zhou, Yi
Keywords: none
MeSH Terms:
  • Animals
  • Cation Transport Proteins/genetics
  • Cation Transport Proteins/metabolism*
  • Eye/metabolism
  • Gene Expression Regulation, Developmental/genetics
  • Gene Expression Regulation, Developmental/physiology*
  • Gene Knockdown Techniques
  • Growth and Development/genetics
  • Growth and Development/physiology*
  • Homeostasis/genetics
  • Homeostasis/physiology*
  • In Situ Hybridization
  • Real-Time Polymerase Chain Reaction
  • Spectrometry, X-Ray Emission
  • Zebrafish/genetics*
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Zinc/metabolism*
PubMed: 22912764 Full text @ PLoS One


Slc39a7/Zip7, also known as Ke4, is a member of solute carrier family 39 (Slc39a) and plays a critical role in regulating cell growth and death. Because the function of Zip7 in vivo was unclear, the present study investigated the function of zip7 in vertebrate development and zinc metabolism using zebrafish as a model organism.

Principal Finding

Using real-time PCR to determine the gene expression pattern of zip7 during zebrafish development, we found that zip7 mRNA is expressed throughout embryonic development and into maturity. Interestingly, whole mount in situ hybridization revealed that while zip7 mRNA is ubiquitously expressed until 12 hours post-fertilization (hpf); at 24 hpf and beyond, zip7 mRNA was specifically detected only in eyes. Morpholino-antisense (MO) gene knockdown assay revealed that downregulation of zip7 expression resulted in several morphological defects in zebrafish including decreased head size, smaller eyes, shorter palates, and shorter and curved spinal cords. Analysis by synchrotron radiation X-ray fluorescence (SR-XRF) showed reduced concentrations of zinc in brain, eyes, and gills of zip7-MO-injected embryos. Furthermore, incubation of the zip7 knockdown embryos in a zinc-supplemented solution was able to rescue the MO-induced morphological defects.


Our data suggest that zip7 is required for eye, brain, and skeleton formation during early embryonic development in zebrafish. Moreover, zinc supplementation can partially rescue defects resulting from zip7 gene knockdown. Taken together, our data provide critical insight into a novel function of zip7 in development and zinc homeostasis in vivo in zebrafish.