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