| Project/Area Number |
62580149
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
代謝生物化学
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| Research Institution | Faculty of Medicine, Osaka University |
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Principal Investigator |
YOSHIDA Yukuo Faculty of Medicine, Osaka University, Assistant, 医学部, 助手 (10144453)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Mitochondria / Protein Transport / Precusor Proteins / ATPaseインヒビター / 15K安定化因子 / プレシーケンス / 安定化因子 / 膜透過 / ホスホリパーゼ |
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| Research Abstract |
Mitochondrial import of an intrinsic ATPase inhibitor and two stabilizing factors, 9K and 15K proteins was investigated. From nucleotide sequences of their genes, the inhibitor and 9K protein were found to have amino terminal presequences as the signals to be targetted by the organelle, while 15K protein had an intramolecular signal but no cleavable presequence. A chemically synthesized presequence of ATPase inhibitor gave rise to transient uncoupling of mitochondrial oxidative phosphorylation. Similar uncoupling was observed with 15K protein denatured by heating in 7M urea, but not with the native protein. During the uncoupling the denatured 15K protein was transported into mitochondria. The uncoupling was blocked by DCCD, but not by olgomycin or atrctyloside. These results suggest that the signal sequence interacts with mitochondrial receptor resulting in opening a H^+ channel and that H^+ influx couples to protein transport into mitochondria.
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