A Mechanism for Mitochondrial DNA Copy Number-regulated Simultaneous Expression of Proteins in Respiratory Complexes.
| Project/Area Number |
23510237
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Genome biology
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| Research Institution | The Institute of Physical and Chemical Research |
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Principal Investigator |
LING Feng 独立行政法人理化学研究所, 吉田化学遺伝学研究室, 専任研究員 (70281665)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 出芽酵母 / DNA組換え / ミトコンドリアDNA / ミトコンドリア融合 / 酸化ストレス応答 / ローリングサークル型複製 / DNA損傷 / Mhr1タンク質 / コンカテマー / DNA二本鎖切断 / 呼吸鎖複合体 / ミトコンドリア / ローリングサークル型DNA複製 / ミトコンドリアヌクレアーゼ / Saccharomyces cerevisiae / mitochondrial fusion / replication / zygote / Concatemer / Rolling-circle type / 遺伝学 / 遺伝子 / 核酸 / ストレス / 品質管理 / DNA複製 |
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| Research Abstract |
We found that mitochondrial fusion induces dissociation of Complex V of the respiratory chain and ROS generation, which increases mitochondrial DNA (mtDNA) copy number in a manner dependent on the homologous DNA pairing protein Mhr1 and also increases in the mtDNA-encoded subunits of Complex V. These results suggested that activation of recombination-dependent replication during mitochondrial fusion plays important roles in maintenance of mitochondrial genomes by preventing generation of mitochondria lacking mtDNA. We further uncovered a mechanism in which relative expression levels of the DNA damage inducible protein Din7 to Mhr1 determine the choice of replication or repair after pairing of homologous DNA by Mhr1.
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Report
(4 results)
Research Products
(18 results)
