C. elegans knockouts in ubiquinone biosynthesis genes result in different phenotypes during larval development

Issue title: The Fourth Conference of the International CoQ10 Association

Article type: Research Article

Authors: Gavilán, Ángela | Asencio, Claudio | Cabello, Juan | Rodríguez-Aguilera, Juan C. | Schnabel, Ralf | Navas, Plácido

Affiliations: Centro Andaluz de Biología del Desarrollo, Departamento de Ciencias Ambientales, Universidad Pablo de Olavide, Ctra. Utrera, Km. 1, E-41013 Sevilla, Spain | Institute of Genetics, Spielmann Strasse 7, TU Braunschweig, 38106 Braunschweig, Germany

Note: [] Corresponding author. Tel.: +1 34 954349385; Fax: +1 34 954349376; E-mail: pnavas@upo.es

Abstract: Ubiquinone is an essential molecule in aerobic organisms to achieve both, ATP synthesis and antioxidant defence. Mutants in genes responsible of ubiquinone biosynthesis lead to non-respiring petite yeast. In C. elegans, coq-7/clk-1 but not coq-3 mutants live longer than wild type showing a 'slowed' phenotype. In this paper we demonstrate that absence in ubiquinone in coq-1, coq-2 or coq-8 mutants lead to larval development arrest, slowed pharyngeal pumping, eventual paralysis and cell death. All these features emerge during larval development, whereas embryo development appeared similar to that of wild type individuals. Dietary coenzyme Q did not restore any of the alterations found in these coq mutants. These phenomena suggest that coenzyme Q mutants unable to synthesize this molecule develop a deleterious phenotype leading to lethality. On the contrary, phenotype of C. elegans coq-7/clk-1 mutants may be a unique phenotype than can not generalize to mutants in ubiquinone biosynthesis. This particular phenotype may not be based on the absence of endogenous coenzyme Q, but to the simultaneous presence of dietary coenzyme Q and the its biosynthesis intermediate demethoxy-coenzyme Q.

Keywords: Coenzyme Q, aging, C. elegans, development

Journal: BioFactors, vol. 25, no. 1-4, pp. 21-29, 2005