title: SLC30A10: A novel manganese transporter.
abstract: Homozygous mutations in SLC30A10 cause familial parkinsonism associated with manganese (Mn) retention. We recently identified SLC30A10 to be a cell surface-localized Mn efflux transporter and demonstrated that parkinsonism-causing mutations block its intracellular trafficking and efflux function. In C. elegans, SLC30A10 over-expression protected against Mn-induced lethality and dopaminergic neurotoxicity, consistent with results in mammalian systems. Here, we present new data about SLC30A10 function in C. elegans. SLC30A10 expression did not protect worms against ZnSO4toxicity, suggesting that SLC30A10 does not mediate Zn export in C. elegans. Furthermore, while a blast search identified 5 potential SLC30A10 homologs in worms (cdf-1, cdf-2, ttm-1 and toc-1; sequence identity <35%), knock-down of these genes showed a tendency of increased survival after Mn exposure (although only ttm-1 was statistically significant), suggesting that the worm homologs may function differently.
authors.affiliation: Department of Molecular Pharmacology; Albert Einstein College of Medicine ; Bronx, NY USA.
authors.forename: Pan
authors.initials: P
authors.lastname: Chen
authors.affiliation: Department of Neurology; Vanderbilt University Medical Center ; Nashville, TN USA.
authors.forename: Aaron B
authors.initials: AB
authors.lastname: Bowman
authors.affiliation: Division of Pharmacology & Toxicology; Institute for Cellular and Molecular Biology and Institute for Neuroscience; College of Pharmacy; The University of Texas at Austin ; Austin, TX USA.
authors.forename: Somshuvra
authors.initials: S
authors.lastname: Mukhopadhyay
authors.affiliation: Department of Molecular Pharmacology; Albert Einstein College of Medicine ; Bronx, NY USA.
authors.forename: Michael
authors.initials: M
authors.lastname: Aschner
keywords: SLC30A10; manganese; neurotoxicity; transporter; zinc