| Project/Area Number |
15K19029
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | ミトコンドリアDNA / 欠失型mtDNAの蓄積 / 線虫 / TFAM / 欠失型ミトコンドリアDNA / mtDNA分配 / ミトコンドリアDNA (mtDNA) / 欠失型mtDNA蓄積 |
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| Outline of Final Research Achievements |
Accumulation of mitochondrial DNA (mtDNA) containing mutation or deletion will be a cause of mitochondrial disease, however, the molecular mechanism and regulating factors in organisms are largely unknown. In this study, we used C. elegans strain LB138 that contains wild-type and deleted mtDNA molecules in heteroplasmic as a model, to identify the regulatory factors in the process. We knocked down several genes that are involved in mtDNA maintenance in LB138. As a result, we found that knockdown of HMG-5, a homologue of human TFAM, significantly reduced the rate of content of deleted mtDNA per wild-type. We then reduced the amount of mtDNA copy number in LB138 by using a replication inhibitor, and examined the effect. The reduction of mtDNA copy number did not significantly affect the mutant rate, suggesting that HMG-5 is involved in stable maintenance of deleted mtDNA molecule independently of the mtDNA copy number maintenance.
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