Copper is an essential nutrient, and deficiency can result in hypopigmentation and neuronal or muscular problems. Deficiency can result from mutations in the copper transporter ATP7A (as in Menkes disease), but many other causes are unknown. Ishizaki et al. take a combined approach to probe biological pathways that are sensitive to copper depletion: they use a zebrafish-based chemical screen to identify compounds affecting copper metabolism, and a yeast genetic screen to map the genetic pathways underlying responsiveness to the compounds. Their results indicate that hypomorphic alleles encoding intracellular trafficking components might underlie sensitivity to reduced copper availability. In addition, this study highlights how disease susceptibility can be influenced by gene-environment networks.

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