|ZFIN ID: ZDB-PUB-110602-24|
Zinc transporter expression in zebrafish (Danio rerio) during development
Ho, E., Dukovcic, S., Hobson, B., Wong, C.P., Miller, G., Hardin, K., Traber, M.G., and Tanguay, R.L.
|Source:||Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 155(1): 26-32 (Journal)|
|Registered Authors:||Tanguay, Robyn L.|
|PubMed:||21596156 Full text @ Comp. Biochem. Physiol. C Toxicol. Pharmacol.|
Ho, E., Dukovcic, S., Hobson, B., Wong, C.P., Miller, G., Hardin, K., Traber, M.G., and Tanguay, R.L. (2012) Zinc transporter expression in zebrafish (Danio rerio) during development. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP. 155(1):26-32.
ABSTRACTZinc is a micronutrient important in several biological processes including growth and development. We have limited knowledge on the impact of maternal zinc deficiency on zinc and zinc regulatory mechanisms in the developing embryo due to a lack of in vivo experimental models that allow us to directly study the effects of maternal zinc on embryonic development following implantation. To overcome this barrier, we have proposed to use zebrafish as a model organism to study the impact of zinc during development. The goal of the current study was to profile the mRNA expression of all the known zinc transporter genes in the zebrafish across embryonic and larval development and to quantify the embryonic zinc concentrations at these corresponding developmental time points. The SLC30A zinc transporter family (ZnT) and SLC39A family, Zir-,Irt-like protein (ZIP) zinc transporter proteins were profiled in zebrafish embryos at 0, 2, 6, 12, 24, 48 and 120h post fertilization to capture expression patterns from a single cell through full development. We observed consistent embryonic zinc levels, but differential expression of several zinc transporters across development. These results suggest that zebrafish is an effective model organism to study the effects of zinc deficiency and further investigation is underway to identify possible molecular pathways that are dysregulated with maternal zinc deficiency.