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Gene Review

clk-1  -  Protein CLK-1

Caenorhabditis elegans

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Disease relevance of clk-1

  • To test the effect of isoprene tail length, N2 and clk-1 animals were fed E. coli engineered to produce Q7, Q8, Q9, or Q10 [1].
  • These results suggest that the uptake and transport of dietary Q(8) to mitochondria prevent the arrest and sterility phenotypes of clk-1 mutants and that DMQ is not functionally equivalent to Q [2].

High impact information on clk-1

  • A cytosolic catalase is needed to extend adult lifespan in C. elegans daf-C and clk-1 mutants [3].
  • The gene clk-1 was identified, and the cloned gene complemented the clk-1 phenotypes and restored normal longevity [4].
  • Inactivation of the Caenorhabditis elegans gene clk-1, which is required for ubiquinone biosynthesis, increases lifespan by an insulin signaling-independent mechanism [5].
  • Mutations in the clk-1 gene of the nematode Caenorhabditis elegans result in an average slowing of a variety of developmental and physiological processes, including the cell cycle, embryogenesis, post-embryonic growth, rhythmic behaviors and aging [6].
  • Three of these genes, age-1, daf-2 and clk-1, have now been cloned [7].

Chemical compound and disease context of clk-1


Biological context of clk-1

  • Mutation in the transcription factor daf-16 suppressed the Age and ATP phenotypes, but not the reduction of respiration rate imparted by mutation in clk-1 [9].
  • Moreover, these mutant alleles both extend life span and increase resistance to ultraviolet (UV) radiation [11], heat [12], and oxidative stress [13-15], though the stress resistance of clk-1 is controversial [10].
  • The differential fertility of clk-1 mutant nematodes fed Q isoforms may result from changes in Q localization, altered recognition by Q-binding proteins, and/or potential defects in mitochondrial function resulting from the mutant CLK-1 polypeptide itself [1].
  • Rates of oxidative phosphorylation were decreased in all three mutants, but the ROS damage was decreased only in clk-1 [11].
  • In contrast, a spe-26 mutant had a tenfold lower mortality until approximately 2 weeks of age but ultimately achieved a higher mortality, whereas clk-1 mutants show slightly higher mortality than wild type during the fertile period, early in life, but ultimately level off at lower mortality [12].

Anatomical context of clk-1

  • The content of Q7 in the mitochondria of clk-1 animals was decreased relative to Q8, suggesting less effective transport of Q7 to the mitochondria, impaired retention, or decreased stability [1].
  • Our results indicate that DMQ9 cannot achieve the same redox role of Q9 in plasma membrane, suggesting that proportion of all these Q isoforms in plasma membrane must be an important factor in establishing the clk-1 mutant phenotype [13].

Associations of clk-1 with chemical compounds


Other interactions of clk-1

  • We tested this hypothesis by measuring respiration rates, light production capacities (a measure of metabolic potential) and ATP levels in various strains harbouring mutant alleles of the Clk genes clk-1 and gro-1 and of three other genes that interact with the Clk genes [9].
  • Each of three well-studied mutants (age-1, clk-1, and spe-26) alters age-specific mortality rates in a fashion unique to itself [17].
  • In C. elegans, coq-7/clk-1 but not coq-3 mutants live longer than wild type showing a 'slowed' phenotype [14].
  • 1. Similarly, there was partial requirement for aak-2 in lifespan extension by mitochondrial mutations (isp-1 and clk-1) [18].
  • In this study, we demonstrated that the daf-2 mutation also conferred an oxidative stress resistance (Oxr) phenotype, which was also enhanced by the clk-1 mutation [19].

Analytical, diagnostic and therapeutic context of clk-1

  • In contrast, we find that food restriction does not further increase the life span of long-lived clk-1 mutants, suggesting that clk-1 and caloric restriction affect similar processes [20].


  1. Reproductive fitness and quinone content of Caenorhabditis elegans clk-1 mutants fed coenzyme Q isoforms of varying length. Jonassen, T., Davis, D.E., Larsen, P.L., Clarke, C.F. J. Biol. Chem. (2003) [Pubmed]
  2. Development and fertility in Caenorhabditis elegans clk-1 mutants depend upon transport of dietary coenzyme Q8 to mitochondria. Jonassen, T., Marbois, B.N., Faull, K.F., Clarke, C.F., Larsen, P.L. J. Biol. Chem. (2002) [Pubmed]
  3. A cytosolic catalase is needed to extend adult lifespan in C. elegans daf-C and clk-1 mutants. Taub, J., Lau, J.F., Ma, C., Hahn, J.H., Hoque, R., Rothblatt, J., Chalfie, M. Nature (2003) [Pubmed]
  4. Structural and functional conservation of the Caenorhabditis elegans timing gene clk-1. Ewbank, J.J., Barnes, T.M., Lakowski, B., Lussier, M., Bussey, H., Hekimi, S. Science (1997) [Pubmed]
  5. Evolutionary conservation of the clk-1-dependent mechanism of longevity: loss of mclk1 increases cellular fitness and lifespan in mice. Liu, X., Jiang, N., Hughes, B., Bigras, E., Shoubridge, E., Hekimi, S. Genes Dev. (2005) [Pubmed]
  6. CLK-1 controls respiration, behavior and aging in the nematode Caenorhabditis elegans. Felkai, S., Ewbank, J.J., Lemieux, J., Labbé, J.C., Brown, G.G., Hekimi, S. EMBO J. (1999) [Pubmed]
  7. Molecular genetics of life span in C. elegans: how much does it teach us? Hekimi, S., Lakowski, B., Barnes, T.M., Ewbank, J.J. Trends Genet. (1998) [Pubmed]
  8. Silencing of ubiquinone biosynthesis genes extends life span in Caenorhabditis elegans. Asencio, C., Rodríguez-Aguilera, J.C., Ruiz-Ferrer, M., Vela, J., Navas, P. FASEB J. (2003) [Pubmed]
  9. Apparent uncoupling of energy production and consumption in long-lived Clk mutants of Caenorhabditis elegans. Braeckman, B.P., Houthoofd, K., De Vreese, A., Vanfleteren, J.R. Curr. Biol. (1999) [Pubmed]
  10. The OLD-1 positive regulator of longevity and stress resistance is under DAF-16 regulation in Caenorhabditis elegans. Murakami, S., Johnson, T.E. Curr. Biol. (2001) [Pubmed]
  11. The effects of complex I function and oxidative damage on lifespan and anesthetic sensitivity in Caenorhabditis elegans. Kayser, E.B., Sedensky, M.M., Morgan, P.G. Mech. Ageing Dev. (2004) [Pubmed]
  12. Age-specific demographic profiles of longevity mutants in Caenorhabditis elegans show segmental effects. Johnson, T.E., Wu, D., Tedesco, P., Dames, S., Vaupel, J.W. J. Gerontol. A Biol. Sci. Med. Sci. (2001) [Pubmed]
  13. Coenzyme Q is irreplaceable by demethoxy-coenzyme Q in plasma membrane of Caenorhabditis elegans. Arroyo, A., Santos-Ocaña, C., Ruiz-Ferrer, M., Padilla, S., Gavilán, A., Rodríguez-Aguilera, J.C., Navas, P. FEBS Lett. (2006) [Pubmed]
  14. C. elegans knockouts in ubiquinone biosynthesis genes result in different phenotypes during larval development. Gavilán, A., Asencio, C., Cabello, J., Rodríguez-Aguilera, J.C., Schnabel, R., Navas, P. Biofactors (2005) [Pubmed]
  15. Mitochondrial oxidative phosphorylation is defective in the long-lived mutant clk-1. Kayser, E.B., Sedensky, M.M., Morgan, P.G., Hoppel, C.L. J. Biol. Chem. (2004) [Pubmed]
  16. Demethoxy-Q, an intermediate of coenzyme Q biosynthesis, fails to support respiration in Saccharomyces cerevisiae and lacks antioxidant activity. Padilla, S., Jonassen, T., Jiménez-Hidalgo, M.A., Fernández-Ayala, D.J., López-Lluch, G., Marbois, B., Navas, P., Clarke, C.F., Santos-Ocaña, C. J. Biol. Chem. (2004) [Pubmed]
  17. Longevity genes in the nematode Caenorhabditis elegans also mediate increased resistance to stress and prevent disease. Johnson, T.E., Henderson, S., Murakami, S., de Castro, E., de Castro, S.H., Cypser, J., Rikke, B., Tedesco, P., Link, C. J. Inherit. Metab. Dis. (2002) [Pubmed]
  18. Aging networks in Caenorhabditis elegans: AMP-activated protein kinase (aak-2) links multiple aging and metabolism pathways. Curtis, R., O'Connor, G., DiStefano, P.S. Aging Cell (2006) [Pubmed]
  19. The daf-2 gene network for longevity regulates oxidative stress resistance and Mn-superoxide dismutase gene expression in Caenorhabditis elegans. Honda, Y., Honda, S. FASEB J. (1999) [Pubmed]
  20. The genetics of caloric restriction in Caenorhabditis elegans. Lakowski, B., Hekimi, S. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
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