Portal de Periódicos da CAPES

Artigo Acesso aberto Produção Nacional Revisado por pares

BIBTEX RIS

Over-expression of COQ10 in Saccharomyces cerevisiae inhibits mitochondrial respiration

2010; Elsevier BV; Volume: 402; Issue: 1 Linguagem: Inglês

10.1016/j.bbrc.2010.09.118

1090-2104

Mariana A. Zampol, Cleverson Busso, Fernando Gomes, José Ribamar Ferreira‐Junior, Alexander Tzagoloff, Mário H. Barros,

Mitochondrial Function and Pathology

COQ10 deletion in Saccharomyces cerevisiae elicits a defect in mitochondrial respiration correctable by addition of coenzyme Q2. Rescue of respiration by Q2 is a characteristic of mutants blocked in coenzyme Q6 synthesis. Unlike Q6 deficient mutants, mitochondria of the coq10 null mutant have wild-type concentrations of Q6. The physiological significance of earlier observations that purified Coq10p contains bound Q6 was examined in the present study by testing the in vivo effect of over-expression of Coq10p on respiration. Mitochondria with elevated levels of Coq10p display reduced respiration in the bc1 span of the electron transport chain, which can be restored with exogenous Q2. This suggests that in vivo binding of Q6 by excess Coq10p reduces the pool of this redox carrier available for its normal function in providing electrons to the bc1 complex. This is confirmed by observing that extra Coq8p relieves the inhibitory effect of excess Coq10p. Coq8p is a putative kinase, and a high-copy suppressor of the coq10 null mutant. As shown here, when over-produced in coq mutants, Coq8p counteracts turnover of Coq3p and Coq4p subunits of the Q-biosynthetic complex. This can account for the observed rescue by COQ8 of the respiratory defect in strains over-producing Coq10p.