ArticleThe Journal of biological chemistry2011
Caenorhabditis elegans UCP4 protein controls complex II-mediated oxidative phosphorylation through succinate transport.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
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- Early Onset of Sex-Dependent Mitochondrial Deficits in the Cortex of 3xTg Alzheimer's Mice.Cells · 2020Article
- Mitochondrial electron transport chain, ROS generation and uncoupling (Review).International journal of molecular medicine · 2019Article
- Axonal Mitochondria Modulate Neuropeptide Secretion Through the Hypoxic Stress Response inGenetics · 2018Article
- The addition of a developmental factor,Biology open · 2017Article
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- The complementary and divergent roles of uncoupling proteins 1 and 3 in thermoregulation.The Journal of physiology · 2016Article
- Uncoupling Protein, UCP-4 May Be Involved in Neuronal Defects During Aging and Resistance to Pathogens in Caenorhabditis elegans.Molecules and cells · 2016Article
- From the Cover: Arsenite Uncouples Mitochondrial Respiration and Induces a Warburg-like Effect in Caenorhabditis elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Perspectives on mitochondrial uncoupling proteins-mediated neuroprotection.Journal of bioenergetics and biomembranes · 2015Review
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- Comparison of proteomic and metabolomic profiles of mutants of the mitochondrial respiratory chain in Caenorhabditis elegans.Mitochondrion · 2015Article
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
The novel uncoupling proteins (UCP2-5) are implicated in the mitochondrial control of oxidant production, insulin signaling, and aging. Attempts to understand their functions have been complicated by overlapping expression patterns in most organisms. Caenorhabditis elegans nematodes are unique because they express only one UCP ortholog, ceUCP4 (ucp4). Here, we performed detailed metabolic analyzes in genetically modified nematodes to define the function of the ceUCP4. The knock-out mutant ucp4 (ok195) exhibited sharply decreased mitochondrial succinate-driven (complex II) respiration. However, respiratory coupling and electron transport chain function were normal in ucp4 mitochondria. Surprisingly, isolated ucp4 mitochondria showed markedly decreased succinate uptake. Similarly, ceUCP4 inhibition blocked succinate respiration and import in wild type mitochondria. Genetic and pharmacologic inhibition of complex I function was selectively lethal to ucp4 worms, arguing that ceUCP4-regulated succinate transport is required for optimal complex II function in vivo. Additionally, ceUCP4 deficiency prolonged lifespan in the short-lived mev1 mutant that exhibits complex II-generated oxidant production. These results identify a novel function for ceUCP4 in the regulation of complex II-based metabolism through an unexpected mechanism involving succinate transport.
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