Transcriptional response to mitochondrial NADH kinase deficiency in Saccharomyces cerevisiae |
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Authors: | Gregory R. Stuart Margaret M. Humble Micheline K. Strand William C. Copeland |
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Affiliation: | 1. Key Laboratory of Conservation Biology for Endangered Wildlife of Ministry of Education and College of Life Sciences, Zhejiang University, Hangzhou 310058, People''s Republic of China;2. School of Chemistry and Material Engineering, Fuyang Teachers College, Fuyang 236037, People''s Republic of China;3. Key Laboratory of Marine Biogenetic Resources, Third Institute of Oceanography, State Oceanic Administration, Xiamen 361005, People''s Republic of China |
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Abstract: | Yeast cells lacking the mitochondrial NADH kinase encoded by POS5 display increased sensitivity to hydrogen peroxide, a slow-growth phenotype, reduced mitochondrial function and increased levels of mitochondrial protein oxidation and mtDNA mutations. Here we examined gene expression in pos5Δ cells, comparing these data to those from cells containing deletions of superoxide dismutase-encoding genes SOD1 or SOD2. Surprisingly, stress–response genes were down-regulated in pos5Δ, sod1Δ and sod2Δ cells, implying that cells infer stress levels from mitochondrial activity rather than sensing reactive oxygen species directly. Additionally, pos5Δ, but not sod1 or sod2, cells displayed an anaerobic expression profile, indicating a defect in oxygen sensing that is specific to pos5, and is not a general stress–response. Finally, the pos5Δ expression profile is quite similar to the hap1Δ expression profile previously reported, which may indicate a shared mechanism. |
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