Over-expression of COQ10 in Saccharomyces cerevisiae inhibits mitochondrial respiration

Autor(es)

Zampol, Mariana A. ^[1] ; Busso, Cleverson ^[1] ; Gomes, Fernando ^[1] ; Ferreira-Junior, Jose Ribamar ^[2] ; Tzagoloff, Alexander ^[3] ; Barros, Mario H. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Ciencias Biomed, Dept Microbiol, BR-05508900 Sao Paulo - Brazil

^[2] Univ Sao Paulo, Escola Artes Ciencias & Humanidades, BR-05508900 Sao Paulo - Brazil

^[3] Columbia Univ, Dept Biol Sci, New York, NY 10027 - USA

• Tipo de documento: Artigo Científico
• Fonte: Biochemical and Biophysical Research Communications; v. 402, n. 1, p. 82-87, NOV 5 2010.
• Citações Web of Science: 16

Resumo

COQ10 deletion in Saccharomyces cerevisiae elicits a defect in mitochondrial respiration correctable by addition of coenzyme Q(2). Rescue of respiration by Q(2) is a characteristic of mutants blocked in coenzyme Q(6) synthesis. Unlike Q(6) deficient mutants, mitochondria of the coq10 null mutant have wild-type concentrations Of Q(6). The physiological significance of earlier observations that purified Coq10p contains bound Q(6) 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 Q(2). This suggests that in vivo binding of Q(6) 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. (C) 2010 Elsevier Inc. All rights reserved. (AU)

• Processo FAPESP: 07/01092-5 - Estudo sobre a montagem dos componentes da cadeia respiratória mitocondrial, estresse oxidativo, e mecanismos regulatórios que levam à sua co-expressão
• Beneficiário: Mario Henrique de Barros
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 06/03713-4 - Biogênese mitocondrial e viabilidade celular: estudo de novos genes envolvidos na expressão funcional da coenzima Q6 de Saccharomyces cerevisae
• Beneficiário: Cleverson Busso
• Modalidade de apoio: Bolsas no Brasil - Doutorado