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Silencing of ubiquinone biosynthesis genes extends life span in Caenorhabditis elegans
Author(s) -
Asencio Claudio,
Rodríguez-Aguilera Juan C.,
Ruiz-Ferrer Macarena,
Vela Jordana,
Navas Plácido
Publication year - 2003
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/fj.02-1022fje
Subject(s) - caenorhabditis elegans , mitochondrion , biology , rna interference , biosynthesis , electron transport chain , gene , coenzyme q – cytochrome c reductase , escherichia coli , gene silencing , biochemistry , microbiology and biotechnology , rna , cytochrome c
Ubiquinone (coenzyme Q; Q) is a key factor in the mitochondria electron transport chain, but it also functions as an antioxidant and as a cofactor of mitochondrial uncoupling proteins. Furthermore, Q isoforms balance in Caenorhabiditis elegans is determined by both dietary intake and endogenous biosynthesis. In the absence of synthesis, withdrawal of dietary Q 8 in adulthood extends life span. Thus, Q plays an important role in the aging process and understanding its synthesis acquires a new impetus. We have identified by RNA interference (RNAi) eight genes, including clk‐1 , involved in ubiquinone biosynthesis in C. elegans feeding animals with dsRNA‐containing Escherichia coli HT115 strains. Silenced C. elegans showed lower levels of both endogenous Q 9 and Q 8 provided by diet, produced less superoxide without a significant modification of mitochondrial electron chain, and extended life span compared with non‐interfered animals. E. coli strains harboring dsRNA also interfered with their own Q 8 biosynthesis. These findings suggest that more efficient electron transport between a lower amount of Q and electron transport capacity of the mitochondrial complexes leads to less production of reactive oxygen species that contributes to extension of life span in the nematode C. elegans .