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Copper is essential for aerobic life, but many aspects of its cellular uptake and distribution remain to be fully elucidated. A genome-wide screen for copper homeostasis genes in  Drosophila melanogaster  identified the SNARE gene  Syntaxin 5  ( Syx5 ) as playing an important role in copper regulation; flies heterozygous for a null mutation in  Syx5  display increased tolerance to high dietary copper. The phenotype is shown here to be due to a decrease in copper accumulation, a mechanism also observed in both  Drosophila  and human cell lines. Studies in adult  Drosophila  tissue suggest that very low levels of  Syx5  result in neuronal defects and lethality, and increased levels also generate neuronal defects. In contrast, mild suppression generates a phenotype typical of copper-deficiency in viable, fertile flies and is exacerbated by co-suppression of the copper uptake gene  Ctr1A . Reduced copper uptake appears to be due to reduced levels at the plasma membrane of the copper uptake transporter, Ctr1. Thus  Syx5  plays an essential role in copper homeostasis and is a candidate gene for copper-related disease in humans.

Syntaxin 5 Is Required for Copper Homeostasis in Drosophila and Mammals