Saccharomyces cerevisiae coq10 null mutants are responsive to antimycin A

Author(s)

Busso, Cleverson ^[1] ; Tahara, Erich B. ^[2] ; Ogusucu, Renata ^[2] ; Augusto, Ohara ^[2] ; Ferreira-Junior, Jose Ribamar ^[3] ; Tzagoloff, Alexander ^[4] ; Kowaltowski, Alicia J. ^[2] ; Barros, Mario H. ^[1]

Affiliation

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

^[2] Univ Sao Paulo, Dept Bioquim, Inst Quim, BR-05508900 Sao Paulo - Brazil

^[3] Univ Sao Paulo, Escola Artes Ciencias & Humanidades, BR-05508900 Sao Paulo - Brazil

^[4] Columbia Univ, Dept Biol Sci, New York, NY 10027 - USA

• Document type: Journal article
• Source: FEBS Journal; v. 277, n. 21, p. 4530-4538, NOV 2010.
• Web of Science Citations: 13

Abstract

Deletion of COQ10 in Saccharomyces cerevisiae elicits a respiratory defect characterized by the absence of cytochrome c reduction, which is correctable by the addition of exogenous diffusible coenzyme Q(2). Unlike other coq mutants with hampered coenzyme Q(6) (Q(6)) synthesis, coq10 mutants have near wild-type concentrations of Q(6). In the present study, we used Q-cycle inhibitors of the coenzyme QH(2)-cytochrome c reductase complex to assess the electron transfer properties of coq10 cells. Our results show that coq10 mutants respond to antimycin A, indicating an active Q-cycle in these mutants, even though they are unable to transport electrons through cytochrome c and are not responsive to myxothiazol. EPR spectroscopic analysis also suggests that wild-type and coq10 mitochondria accumulate similar amounts of Q(6) semiquinone, despite a lower steady-state level of coenzyme QH(2)-cytochrome c reductase complex in the coq10 cells. Confirming the reduced respiratory chain state in coq10 cells, we found that the expression of the Aspergillus fumigatus alternative oxidase in these cells leads to a decrease in antimycin-dependent H(2)O(2) release and improves their respiratory growth. (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