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Papers In Press, published online ahead of print September 24, 2002
Department of Chemistry and Biochemistry, UCLA, Los Angeles, CA 90095-1569
Corresponding Author: larsen{at}chem.ucla.edu
The C. 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 E. 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 However, if Q is withdrawn from the diet, clk-1 animals either arrest development as young larvae or become sterile adults depending upon the stage at the time of the withdrawal.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 prevents the arrest and sterility phenotypes of clk-1 mutants and that DMQ is not functionally equivalent to Q.
J. Biol. Chem, 10.1074/jbc.M204758200
Submitted on May 15, 2002
Revised on September 24, 2002
Accepted on September 24, 2002
Development and fertility in C. elegans clk-1 mutants depends upon transport of dietary coenzyme Q8 to mitochondria
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