Development and fertility in Caenorhabditis elegans clk-1 mutants depend upon transport of dietary coenzyme Q8 to mitochondria

Tanya Jonassen, Beth N. Marbois, Kym F. Faull, Catherine F. Clarke, Pamela L. Larsen

Research output: Contribution to journalArticlepeer-review

78 Scopus citations


The Caenorhabditis elegans clk-1 mutants lack coenzyme Q9 and instead accumulate the biosynthetic intermediate demethoxy-Q9 (DMQ9). clk-1 animals grow to reproductive adults, albeit slowly, if supplied with Q8-containing Escherichia coli. However, if Q is withdrawn from the diet, clk-1 animals either arrest development as young larvae or become sterile adults depending upon the stage at the time of the withdrawal. To understand this stage-dependent response to a Q-less diet, the quinone content was determined during development of wild-type animals. The quinone content varies in the different developmental stages in wild-type fed Q8-replete E. coli. The amounts peak at the second larval stage, which coincides with the stage of arrest of clk-1 larvae fed a Q-less diet from hatching. Levels of the endogenously synthesized DMQ9 are high in the clk-1(qm30)-arrested larvae and sterile adults fed Q-less food. Comparison of quinones from animals fed a Q-replete or a Q-less diet establishes that the Q8 present is assimilated from the E. coli. Furthermore, this E. coli-specific Q8 is present in mitochondria isolated from fertile clk-1(qm30) adults fed a Q-replete diet. These results suggest that the uptake and transport of dietary Q8 to mitochondria prevent the arrest and sterility phenotypes of clk-1 mutants and that DMQ is not functionally equivalent to Q.

Original languageEnglish (US)
Pages (from-to)45020-45027
Number of pages8
JournalJournal of Biological Chemistry
Issue number47
StatePublished - Nov 22 2002
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Biochemistry
  • Cell Biology


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