ArticlePLoS genetics2014
The Caenorhabditis elegans iodotyrosine deiodinase ortholog SUP-18 functions through a conserved channel SC-box to regulate the muscle two-pore domain potassium channel SUP-9.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 0 citations in OpenAlex.
- A leak KPNAS nexus · 2024Article
- Differential modulation of C. elegans motor behavior by NALCN and two-pore domain potassium channels.PLoS genetics · 2022Article
- The minimal structure for iodotyrosine deiodinase function is defined by an outlier protein from the thermophilic bacterium Thermotoga neapolitana.The Journal of biological chemistry · 2021Article
- Evolutionary aspects of the Viridiplantae nitroreductases.Journal, genetic engineering & biotechnology · 2020Article
- Mutation of a single residue promotes gating of vertebrate and invertebrate two-pore domain potassium channels.Nature communications · 2019Article
- The distribution and mechanism of iodotyrosine deiodinase defied expectations.Archives of biochemistry and biophysics · 2017Review
- Complex Locomotion Behavior Changes Are Induced in Caenorhabditis elegans by the Lack of the Regulatory Leak K+ Channel TWK-7.Genetics · 2016Article
- The BLI-3/TSP-15/DOXA-1 dual oxidase complex is required for iodide toxicity in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2014Article
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Authors and funding
3 authors at 3 institutions in 2 countries.
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Abstract
Loss-of-function mutations in the Caenorhabditis elegans gene sup-18 suppress the defects in muscle contraction conferred by a gain-of-function mutation in SUP-10, a presumptive regulatory subunit of the SUP-9 two-pore domain K(+) channel associated with muscle membranes. We cloned sup-18 and found that it encodes the C. elegans ortholog of mammalian iodotyrosine deiodinase (IYD), an NADH oxidase/flavin reductase that functions in iodine recycling and is important for the biosynthesis of thyroid hormones that regulate metabolism. The FMN-binding site of mammalian IYD is conserved in SUP-18, which appears to require catalytic activity to function. Genetic analyses suggest that SUP-10 can function with SUP-18 to activate SUP-9 through a pathway that is independent of the presumptive SUP-9 regulatory subunit UNC-93. We identified a novel evolutionarily conserved serine-cysteine-rich region in the C-terminal cytoplasmic domain of SUP-9 required for its specific activation by SUP-10 and SUP-18 but not by UNC-93. Since two-pore domain K(+) channels regulate the resting membrane potentials of numerous cell types, we suggest that the SUP-18 IYD regulates the activity of the SUP-9 channel using NADH as a coenzyme and thus couples the metabolic state of muscle cells to muscle membrane excitability.
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