Biophysical characterization of the iron in mitochondria from Atm1p-depleted Saccharomyces cerevisiae
| Autor: | E. Ann Ellis, Robert A. Scott, Hansoo Kim, Paul A. Lindahl, Ren Miao, Uma Mahendra Kumar Koppolu |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Iron-Sulfur Proteins
Saccharomyces cerevisiae Proteins Iron Saccharomyces cerevisiae Heme Mitochondrion Biochemistry Article chemistry.chemical_compound Spectroscopy Mossbauer Ferrous Compounds Inner mitochondrial membrane Ferredoxin chemistry.chemical_classification Reactive oxygen species biology Electron Spin Resonance Spectroscopy biology.organism_classification Aerobiosis Cytosol Microscopy Electron Oxidative Stress X-Ray Absorption Spectroscopy chemistry Mitochondrial Membranes Frataxin biology.protein ATP-Binding Cassette Transporters Spectrophotometry Ultraviolet |
| Zdroj: | Biochemistry. 48(40) |
| ISSN: | 1520-4995 |
| Popis: | Atm1p is an ABC transporter localized in the mitochondrial inner membrane; it functions to export an unknown species into the cytosol and is involved in cellular iron metabolism. Depletion or deletion of Atm1p causes Fe accumulation in mitochondria and a defect in cytosolic Fe/S cluster assembly, but reportedly not a defect in mitochondrial Fe/S cluster assembly. In this study the nature of the accumulated Fe was examined using Mössbauer spectroscopy, EPR, electronic absorption spectroscopy, X-ray absorption spectroscopy, and electron microscopy. The Fe that accumulated in aerobically grown cells was in the form of Fe(III) phosphate nanoparticles similar to that which accumulates in yeast frataxin Yfh1p-deleted or yeast ferredoxin Yah1p-depleted cells. Relative to WT mitochondria, Fe/S cluster and heme levels in Atm1p-depleted mitochondria from aerobic cells were significantly diminished. Atm1p-depletion also caused a build-up of nonheme Fe(II) ions in the mitochondria and an increase in oxidative damage. Atm1p-depleted mitochondria isolated from anaerobically grown cells exhibited WT levels of Fe/S clusters and hemes, and they did not hyper-accumulate Fe. Atm1p-depleted cells lacked Leu1p activity, regardless of whether they were grown aerobically or anaerobically. These results indicate that Atm1p does not participate in mitochondrial Fe/S cluster assembly, and that the species exported by Atm1p is required for cytosolic Fe/S cluster assembly. The Fe/S cluster defect and the Fe-accumulation phenotype, resulting from the depletion of Atm1p in aerobic cells (but not in anaerobic cells), may be secondary effects that are observed only when cells are exposed to oxygen during growth. Reactive oxygen species generated under these conditions might degrade iron-sulfur clusters and lower heme levels in the organelle. |
| Databáze: | OpenAIRE |
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