{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T10:40:04Z","timestamp":1782124804440,"version":"3.54.5"},"reference-count":63,"publisher":"The Company of Biologists","issue":"9-10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,9,1]]},"abstract":"<jats:title>SUMMARY<\/jats:title>\n               <jats:p>Hypopigmentation is a feature of copper deficiency in humans, as caused by mutation of the copper (Cu2+) transporter ATP7A in Menkes disease, or an inability to absorb copper after gastric surgery. However, many causes of copper deficiency are unknown, and genetic polymorphisms might underlie sensitivity to suboptimal environmental copper conditions. Here, we combined phenotypic screens in zebrafish for compounds that affect copper metabolism with yeast chemical-genetic profiles to identify pathways that are sensitive to copper depletion. Yeast chemical-genetic interactions revealed that defects in intracellular trafficking pathways cause sensitivity to low-copper conditions; partial knockdown of the analogous Ap3s1 and Ap1s1 trafficking components in zebrafish sensitized developing melanocytes to hypopigmentation in low-copper environmental conditions. Because trafficking pathways are essential for copper loading into cuproproteins, our results suggest that hypomorphic alleles of trafficking components might underlie sensitivity to reduced-copper nutrient conditions. In addition, we used zebrafish-yeast screening to identify a novel target pathway in copper metabolism for the small-molecule MEK kinase inhibitor U0126. The zebrafish-yeast screening method combines the power of zebrafish as a disease model with facile genome-scale identification of chemical-genetic interactions in yeast to enable the discovery and dissection of complex multigenic interactions in disease-gene networks.<\/jats:p>","DOI":"10.1242\/dmm.005769","type":"journal-article","created":{"date-parts":[[2010,8,17]],"date-time":"2010-08-17T01:55:12Z","timestamp":1282010112000},"page":"639-651","source":"Crossref","is-referenced-by-count":38,"title":["Combined zebrafish-yeast chemical-genetic screens reveal gene\u2013copper-nutrition interactions that modulate melanocyte pigmentation"],"prefix":"10.1242","volume":"3","author":[{"given":"Hironori","family":"Ishizaki","sequence":"first","affiliation":[{"name":"Institute of Genetics and Molecular Medicine, MRC Human Genetics Unit and The University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michaela","family":"Spitzer","sequence":"additional","affiliation":[{"name":"Wellcome Trust Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King\u2019s Buildings, Mayfield Road, Edinburgh, EH9 3JR, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Wildenhain","sequence":"additional","affiliation":[{"name":"Wellcome Trust Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King\u2019s Buildings, Mayfield Road, Edinburgh, EH9 3JR, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Corina","family":"Anastasaki","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Molecular Medicine, MRC Human Genetics Unit and The University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiqiang","family":"Zeng","sequence":"additional","affiliation":[{"name":"Institute of Genetics and Molecular Medicine, MRC Human Genetics Unit and The University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sonam","family":"Dolma","sequence":"additional","affiliation":[{"name":"Center for Systems Biology, Samuel Lunenfeld Research Institute, 600 University Avenue, Toronto, Ontario, M5G 1X5, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Shaw","sequence":"additional","affiliation":[{"name":"Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"Madsen","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan","family":"Gitlin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Marais","sequence":"additional","affiliation":[{"name":"The Institute of Cancer Research, Signal Transduction Team, Section of Cell and Molecular Biology, 237 Fulham Road, London, SW3 6JB, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mike","family":"Tyers","sequence":"additional","affiliation":[{"name":"Wellcome Trust Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King\u2019s Buildings, Mayfield Road, Edinburgh, EH9 3JR, UK"},{"name":"Center for Systems Biology, Samuel Lunenfeld Research Institute, 600 University Avenue, Toronto, Ontario, M5G 1X5, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. 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