Genetic and molecular characterization of CLK-1/mCLK1, a conserved determinant of the rate of aging

Exp Gerontol. 2006 Oct;41(10):940-51. doi: 10.1016/j.exger.2006.06.041. Epub 2006 Aug 4.


The clk-1 gene of the nematode Caenorhabditis elegans encodes an evolutionarily conserved enzyme that is necessary for ubiquinone biosynthesis. Loss-of-function mutations in clk-1, as well as in its mouse orthologue mclk1, increase lifespan in both organisms. In nematodes, clk-1 extends lifespan by a mechanism that is distinct from the insulin signaling-like pathway but might have similarities to calorie restriction. The evolutionary conservation of the effect of clk-1/mclk1 on lifespan suggests that the gene affects a fundamental mechanism of aging. The clk-1/mclk1 system could allow for the understanding of this mechanism by combining genetic and molecular investigations in worms with studies in mice, where age-dependent disease processes relevant to human health can be modeled.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging / genetics*
  • Animals
  • Caenorhabditis elegans / genetics
  • Caenorhabditis elegans Proteins / genetics*
  • Diet
  • Humans
  • Lipid Metabolism / genetics
  • Longevity / genetics
  • Loss of Heterozygosity / genetics
  • Membrane Proteins / genetics*
  • Mice
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / metabolism
  • Mixed Function Oxygenases
  • Mutation
  • Phenotype
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / genetics
  • Temperature
  • Ubiquinone / administration & dosage
  • Ubiquinone / biosynthesis
  • Ubiquinone / metabolism


  • CLK-1 protein, C elegans
  • Caenorhabditis elegans Proteins
  • Membrane Proteins
  • Mitochondrial Proteins
  • Reactive Oxygen Species
  • Ubiquinone
  • Mixed Function Oxygenases
  • Coq7 protein, mouse