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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Over-expression of COQ10 in Saccharomyces cerevisiae inhibits mitochondrial respiration

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Author(s):
Zampol, Mariana A. [1] ; Busso, Cleverson [1] ; Gomes, Fernando [1] ; Ferreira-Junior, Jose Ribamar [2] ; Tzagoloff, Alexander [3] ; Barros, Mario H. [1]
Total Authors: 6
Affiliation:
[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
Total Affiliations: 3
Document type: Journal article
Source: Biochemical and Biophysical Research Communications; v. 402, n. 1, p. 82-87, NOV 5 2010.
Web of Science Citations: 16
Abstract

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)

FAPESP's process: 07/01092-5 - Assembly of respiratory chain complexes, oxidative stress and regulatory mechanisms involved in their co-expression
Grantee:Mario Henrique de Barros
Support Opportunities: Regular Research Grants