ArticleThe Journal of biological chemistry2017
The Intestinal Copper Exporter CUA-1 Is Required for Systemic Copper Homeostasis in Caenorhabditis elegans.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- A conserved vesicular circuit enables metabolic adaptation and maintains systemic heme homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Cuproptosis inducers mediate cold lethality via SLCR-46.1 in C. elegans.Nature communications · 2026Article
- Review
- Repurposing melatonin's therapeutic potential in Wilson disease: Addressing copper overload and redox imbalance.Redox biology · 2026Article
- The 3D Ultrastructure ofmicroPublication biology · 2026Article
- A C. elegans model of copper deficiency: Dietary interventions rescue CTR1/CHCA-1 copper transporter mutant phenotype.PLoS genetics · 2026Article
- Blue light stimulated-autofluorescence green flash of lysosome-related organelles in the intestinal cells of nematodes.G3 (Bethesda, Md.) · 2025Article
- Blue light stimulated-autofluorescence green flash of lysosome-related organelles in the intestinal cells of nematodes.bioRxiv : the preprint server for biology · 2025Article
- Exogenous prion-like proteins and their potential to trigger cognitive dysfunction.Molecular systems biology · 2025Article
- Some Properties of theInternational journal of molecular sciences · 2025Article
- A histochemical approach to activity-based copper sensing reveals cuproplasia-dependent vulnerabilities in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- LYSMD proteins promote activation of Rab32-family GTPases for lysosome-related organelle biogenesis.The Journal of cell biology · 2024Article
- GlialProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Single-tissue proteomics inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Small-Molecule Fluorescent Probes for Binding- and Activity-Based Sensing of Redox-Active Biological Metals.Chemical reviews · 2024Review
- Copper Homeostasis in the Model OrganismCells · 2024Review
- Lysosome-related organelles contain an expansion compartment that mediates delivery of zinc transporters to promote homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A new Caenorhabditis elegans model to study copper toxicity in Wilson disease.Traffic (Copenhagen, Denmark) · 2024Article
- Dysfunction in atox-1 and ceruloplasmin alters labile Cu levels and consequently Cu homeostasis inFrontiers in molecular biosciences · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper plays key catalytic and regulatory roles in biochemical processes essential for normal growth, development, and health. Defects in copper metabolism cause Menkes and Wilson's disease, myeloneuropathy, and cardiovascular disease and are associated with other pathophysiological states. Consequently, it is critical to understand the mechanisms by which organisms control the acquisition, distribution, and utilization of copper. The intestinal enterocyte is a key regulatory point for copper absorption into the body; however, the mechanisms by which intestinal cells transport copper to maintain organismal copper homeostasis are poorly understood. Here, we identify a mechanism by which organismal copper homeostasis is maintained by intestinal copper exporter trafficking that is coordinated with extraintestinal copper levels in Caenorhabditis elegans Specifically, we show that CUA-1, the C. elegans homolog of ATP7A/B, localizes to lysosome-like organelles (gut granules) in the intestine under copper overload conditions for copper detoxification, whereas copper deficiency results in a redistribution of CUA-1 to basolateral membranes for copper efflux to peripheral tissues. Worms defective in gut granule biogenesis exhibit defects in copper sequestration and increased susceptibility to toxic copper levels. Interestingly, however, a splice isoform CUA-1.2 that lacks a portion of the N-terminal domain is targeted constitutively to the basolateral membrane irrespective of dietary copper concentration. Our studies establish that CUA-1 is a key intestinal copper exporter and that its trafficking is regulated to maintain systemic copper homeostasis. C. elegans could therefore be exploited as a whole-animal model system to study regulation of intra- and intercellular copper trafficking pathways.
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