Abstract
Mutations in the clk-1 gene of Caenorhabditis elegans extend worm life span and slow down a variety of physiological processes. Here we report that C. elegans CLK-1 as well as its mouse homologue have DNA binding activity that is specific to the O(L) region of mitochondrial DNA. DNA binding activity of CLK-1 is inhibited by ADP, and is altered by mutations that extend nematode life span. Our results suggest that, in addition to its enzymatic function in ubiquinone biosynthesis, CLK-1 is involved in the regulation of mtDNA replication or transcription.
MeSH terms
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Adenosine Diphosphate / pharmacology
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Animals
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Base Sequence
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Binding Sites / genetics
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Caenorhabditis elegans / genetics
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Caenorhabditis elegans / physiology
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Caenorhabditis elegans Proteins / chemistry
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Caenorhabditis elegans Proteins / genetics
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Caenorhabditis elegans Proteins / metabolism*
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DNA, Helminth / chemistry
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DNA, Helminth / genetics
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DNA, Helminth / metabolism*
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DNA, Mitochondrial / chemistry
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DNA, Mitochondrial / genetics
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DNA, Mitochondrial / metabolism*
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DNA-Binding Proteins / chemistry
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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Genes, Helminth
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Helminth Proteins / chemistry
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Helminth Proteins / genetics
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Helminth Proteins / metabolism*
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In Vitro Techniques
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Longevity / genetics
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Longevity / physiology
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Membrane Proteins / chemistry
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Membrane Proteins / genetics
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Membrane Proteins / metabolism
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Mice
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Mitochondrial Proteins
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Mixed Function Oxygenases
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Mutation
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Nucleic Acid Conformation
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Recombinant Proteins / chemistry
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Recombinant Proteins / genetics
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Recombinant Proteins / metabolism
Substances
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CLK-1 protein, C elegans
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Caenorhabditis elegans Proteins
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DNA, Helminth
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DNA, Mitochondrial
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DNA-Binding Proteins
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Helminth Proteins
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Membrane Proteins
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Mitochondrial Proteins
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Recombinant Proteins
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Adenosine Diphosphate
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Mixed Function Oxygenases
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Coq7 protein, mouse