Mitochondrial efficiency-dependent viability of saccharomyces cerevisiae mutants carrying individual electron transport chain component deletions

Young Yon Kwon, Kyung Mi Choi, Chang Yeon Cho, Cheol-Koo Lee

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8 Citations (Scopus)


Mitochondria play a crucial role in eukaryotic cells; the mitochondrial electron transport chain (ETC) generates adenosine triphosphate (ATP), which serves as an energy source for numerous critical cellular activities. However, the ETC also generates deleterious reactive oxygen species (ROS) as a natural byproduct of oxidative phosphorylation. ROS are considered the major cause of aging because they damage proteins, lipids, and DNA by oxidation. We analyzed the chronological life span, growth phenotype, mitochondrial membrane potential (MMP), and intracellular ATP and mitochondrial superoxide levels of 33 single ETC component-deleted strains during the chronological aging process. Among the ETC mutant strains, 14 (sdh1Δ, sdh2Δ, sdh4Δ, cor1Δ, cyt1Δ, qcr7Δ, qcr8Δ, rip1Δ, cox6Δ, cox7Δ, cox9Δ, atp4Δ, atp7Δ, and atp17Δ) showed a significantly shorter life span. The deleted genes encode important elements of the ETC components succinate dehydrogenase (complex II) and cytochrome c oxidase (complex IV), and some of the deletions lead to structural instability of the membrane-F1F0- ATP synthase due to mutations in the stator stalk (complex V). These short-lived strains generated higher superoxide levels and produced lower ATP levels without alteration of MMP. In summary, ETC mutations decreased the life span of yeast due to impaired mitochondrial efficiency.

Original languageEnglish
Pages (from-to)1054-1063
Number of pages10
JournalMolecules and Cells
Issue number12
Publication statusPublished - 2015 Nov 24



  • Cellular ATP
  • Electron transport chain
  • ETC-component single gene deletion
  • Mitochondria
  • Mitochondrial ROS

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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