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Characterizing a coq‐3 mutation that extends life span in C. elegans
Author(s) -
Gomez Fernando,
Saiki Ryoichi,
Chin Randall,
Srinivasan Chandra,
Clarke Catherine F.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.660.1
Subject(s) - mutant , biology , wild type , gene , genetics , mutation , microbiology and biotechnology
Coenzyme Q (referred to simply as Q) is a lipophilic component of the electron transport chain in mitochondria. The biosynthesis of Q is known to include several steps, including two O ‐methyltransferase reactions catalyzed by COQ‐3. Expression of C. elegan s COQ‐3 restores respiratory growth and Q biosynthesis in an E. coli ubiG mutant. In C. elegans, coq‐3 mutants demonstrate altered fertility and survival. One mutant, coq‐3(qm188) , is sterile. Another mutant, coq‐3(ok506) , is fertile. Both mutant strains are sterile when fed the Q‐deficient bacteria strain GD‐1. Western blot analyses with a COQ‐3 protein antibody indicate that both mutants also lack the wild‐type protein. The coq‐3 gene is situated in a three‐gene operon. QT‐PCR analysis shows that transcript levels of the upstream gene, nuo‐3 , in coq‐3(qm188) mutants are widely variant compared to wild‐type and coq‐3(ok506) mutants. This erratic expression pattern indicates that coq‐3(qm188) is not a representative coq‐3 mutant. Mutant coq‐3(ok506) raised on the Q‐less E. coli strain GD1 possess small, thin and severely underdeveloped gonads, and live 125% longer than wild‐type worms raised on a this diet. Mutants raised on OP50 have a 40% shorter life span than wild type worms and an asymmetrical uterine anatomy. Since uterine physiology affects life span, our anatomical data may help explain why coq‐3(ok506) homozygotes raised on GD1 live longer,