2005 Fiscal Year Final Research Report Summary
Roles of mitochondrial proteins in regulations of energy metabolism and apoptosis
| Project/Area Number |
14370746
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | The University of Tokushima |
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Principal Investigator |
SHINOHARA Yasuo The University of Tokushima, Institute for Genome Research, Professor, ゲノム機能研究センター, 教授 (60226157)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAZAKI Naoshi The University of Tokushima, Institute of Health Biosciences, Assistant Professor, 大学院・ヘルスバイオサイエンス研究部, 助手 (20271083)
TERADA Hiroshi Tokyo University of Science, Faculty of Pharmaceutical Sciences, Professor, 薬学部, 教授 (00035544)
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| Project Period (FY) |
2002 – 2005
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| Keywords | mitochondria / apoptosis / permeability transition / cytochrome c / proteomics analysis / energy conversion / Yeast |
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| Research Abstract |
Mitochondria are known to be a major site of cellular energy conversion. However, recent studies demonstrated that mitochondria are not only functioning as a site of energy conversion, but also as a regulatory site of cellular fate. Control of cellular fate by mitochondria is known to be regulated by controlling the release of mitochondrial cytochrome c into the cytosol. When cellular signals of apoptosis are delivered into the mitochondria, dysfunction of mitochondria is induced and mitochondrial cytochrome c is released from mitochondria. Cytochrome c thus released into cytosol triggers subsequent steps of cellular apoptosis. However, mechanisms how mitochondrial cytochrome c is released from mitochondria are still uncertain.
In the present study, to understand the molecular mechanisms controlling release of mitochondrial cytochrome c, relationship between mitochondrial dysfunction and release of mitochondrial cytochrome c was investigated. As a result, release of mitochondrial cytochrome c was found to be independent process from the dysfunction of mitochondria.
Furthermore, to understand the roles of mitochondrial proteins in the regulation of release of mitochondrial cytochrome c, experimental system using yeast cells was established. Our results clearly indicated that yeast mitochondria could be utilize as a nice model system of mammalian mitochondria, because dysfunction of yeast mitochondria caused release of mitochondrial cytochrome c likewise mammalian mitochondria.
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