ArticleACS chemical neuroscience2019
SLC30A10 Mutation Involved in Parkinsonism Results in Manganese Accumulation within Nanovesicles of the Golgi Apparatus.
Article in ACS chemical neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- Synchrotron XRF Imaging Reveals Manganese Accumulation in the Golgi and Post-Synapses of Neurons and Enhanced Uptake in Astrocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Manganese Neurotoxicity and Familial Disorders of Manganese Transport.Annals of the Child Neurology Society · 2025Review
- Studies of Slc30a10 Deficiency in Mice Reveal That Intestinal Iron Transporters Dmt1 and Ferroportin Transport Manganese.Cellular and molecular gastroenterology and hepatology · 2025Article
- Native Cryo-Correlative Light and Synchrotron X-ray Fluorescence Imaging of Proteins and Essential Metals in Subcellular Neuronal Compartments.Chemical & biomedical imaging · 2024Article
- Manganese transporter SLC30A10 and iron transporters SLC40A1 and SLC11A2 impact dietary manganese absorption.bioRxiv : the preprint server for biology · 2024Article
- A water-soluble, cell-permeable Mn(ii) sensor enables visualization of manganese dynamics in live mammalian cells.Chemical science · 2024Article
- The organization and function of the Golgi apparatus in dendrite development and neurological disorders.Genes & diseases · 2023Review
- Exposing the role of metals in neurological disorders: a focus on manganese.Trends in molecular medicine · 2022Review
- Review
- Dose-efficient multimodal microscopy of human tissue at a hard X-ray nanoprobe beamline.Journal of synchrotron radiation · 2022Article
- Article
- Abridged spectral matrix inversion: parametric fitting of X-ray fluorescence spectra following integrative data reduction.Journal of synchrotron radiation · 2021Article
- Characterization of in vitro models of SLC30A10 deficiency.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021Article
- X-ray-Based Techniques to Study the Nano-Bio Interface.ACS nano · 2021Article
- Transmembrane 163 (TMEM163) Protein: A New Member of the Zinc Efflux Transporter Family.Biomedicines · 2021Review
- Article
- Multivalent ions and biomolecules: Attempting a comprehensive perspective.Chemphyschem : a European journal of chemical physics and physical chemistry · 2020Review
- Nano-imaging trace elements at organelle levels in substantia nigra overexpressing α-synuclein to model Parkinson's disease.Communications biology · 2020Article
- Advances in visualization of copper in mammalian systems using X-ray fluorescence microscopy.Current opinion in chemical biology · 2020Review
- ZIP14 is degraded in response to manganese exposure.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2019Article
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Manganese (Mn) is an essential metal that can be neurotoxic when elevated exposition occurs leading to parkinsonian-like syndromes. Mutations in the Slc30a10 gene have been identified in new forms of familial parkinsonism. SLC30A10 is a cell surface protein involved in the efflux of Mn and protects the cell against Mn toxicity. Disease-causing mutations block the efflux activity of SLC30A10, resulting in Mn accumulation. Determining the intracellular localization of Mn when disease-causing SLC30A10 mutants are expressed is essential to elucidate the mechanisms of Mn neurotoxicity. Here, using organelle fluorescence microscopy and synchrotron X-ray fluorescence (SXRF) imaging, we found that Mn accumulates in the Golgi apparatus of human cells transfected with the disease-causing SLC30A10-Δ105-107 mutant under physiological conditions and after exposure to Mn. In cells expressing the wild-type SLC30A10 protein, cellular Mn content was low after all exposure conditions, confirming efficient Mn efflux. In nontransfected cells that do not express endogenous SLC30A10 and in mock transfected cells, Mn was located in the Golgi apparatus, similarly to its distribution in cells expressing the mutant protein, confirming deficient Mn efflux. The newly developed SXRF cryogenic nanoimaging (<50 nm resolution) indicated that Mn was trapped in single vesicles within the Golgi apparatus. Our results confirm the role of SLC30A10 in Mn efflux and the accumulation of Mn in cells expressing the disease-causing SLC30A10-Δ105-107 mutation. Moreover, we identified suborganelle Golgi nanovesicles as the main compartment of Mn accumulation in SLC30A10 mutants, suggesting interactions with the vesicular trafficking machinery as a cause of the disease.
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