Zinc is an abundant and essential dietary nutrient required as an enzymatic or structural cofactor for many proteins. As such, the cellular distribution of zinc ions must be tightly regulated to ensure adequate supply to each cellular organelle while avoiding potential toxicity due to competition with other essential metal ions Transport of zinc ions between and within cells is mediated by members of the Zip (SLC39) and ZnT (SLC30) families of transmembrane domain proteins. The genome of the vinegar fly Drosophila melanogaster encodes ten Zip proteins and seven ZnT families, with clear homologues of each of the twenty-four mammalian Zip and ZnT proteins. The tools available for functional genetic analysis in Drosophila make it an excellent system in which to investigate the in vivo roles of each of these zinc transporters and how they interact at the cellular and systemic levels.

Previously, we have carried out a systematic analysis of Zip and ZnT gene function in the fly¹  and identified a cellular zinc toxicity phenotype which we then used to detect more subtle zinc transport activities in the developing fly eye² . Here, we extend this work, presenting additional zinc toxicity and zinc deficiency phenotypes which represent mislocalization of zinc in specific cellular organelles. This work will be supported by a detailed investigation of the in vivo subcellular localization of each zinc transporter, quantification of cellular zinc distribution using zinc fluorophores and an examination of how each of the transporters impacts on the zinc dyshomeostasis phenotypes. Preliminary findings from a pilot genetic modifier screen aimed at identifying additional zinc homeostasis genes will also be presented.