Syntaxin 5 is required for copper homeostasis in Drosophila and mammals

Norgate, Melanie, Southon, Adam, Greenough, Mark, Cater, Michael, Farlow, Ashley, Batterham, Philip, Bush Ashley I., Subramaniam, V. Nathan, Burke, Richard and Camakaris, James (2010) Syntaxin 5 is required for copper homeostasis in Drosophila and mammals. PLoS One, 5 12: e14303-1-e14303-10. doi:10.1371/journal.pone.0014303

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Author Norgate, Melanie
Southon, Adam
Greenough, Mark
Cater, Michael
Farlow, Ashley
Batterham, Philip
Bush Ashley I.
Subramaniam, V. Nathan
Burke, Richard
Camakaris, James
Title Syntaxin 5 is required for copper homeostasis in Drosophila and mammals
Formatted title
Syntaxin 5 is required for copper homeostasis in Drosophila and mammals
Journal name PLoS One   Check publisher's open access policy
ISSN 1932-6203
Publication date 2010-12-20
Year available 2010
Sub-type Article (original research)
DOI 10.1371/journal.pone.0014303
Open Access Status DOI
Volume 5
Issue 12
Start page e14303-1
End page e14303-10
Total pages 10
Editor Joanna Mary Bridger
Place of publication San Francisco, CA, U.S.A.
Publisher Public Library of Science (PLoS)
Language eng
Formatted abstract
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.
© 2010 Norgate et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Keyword Multidisciplinary Sciences
Science & Technology - Other Topics
Q-Index Code C1
Q-Index Status Confirmed Code
Grant ID DP0451599
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2011 Collection
School of Medicine Publications
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