| Nuclear and mitochondrial genome responses in HeLa cells treated with inhibitors of mitochondrial DNA expression. | |
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MedLine Citation:
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PMID: 16951738 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The influence of mutations in the mitochondrial DNA (mtDNA) on the bioenergetic metabolism of the cell is still poorly understood. Many of the mutations in the mtDNA affect the expression of the mitochondrial genome. Investigations on cells from patients are not easy, especially as the mitochondrial DNA is heteroplasmic and this state is changed in culture. Moreover, the nuclear background and the mitochondrial haplotype may affect the behaviour of cells. Transfer of patient mitochondria to rho zero cell lines is also not optimal as these cells in general have many nuclear changes which may also affect cell behaviour. Thus, we decided to use inhibitors of mitochondrial genome expression, such as thiamphenicol, ethidium bromide and dideoxycytidine to investigate the bioenergetic metabolism of HeLa cells. We found that oxidative phosphorylation and glycolysis participate equally in ATP production in HeLa cells and that decreased activity of the respiratory chain leads to increased glycolysis and the reduction of cell growth. Insufficient ATP production in the oxidative phosphorylation process was not compensated by increased proliferation of the mitochondria. However, we were able to show that there are some mechanisms compensating limited expression of the mitochondrial genome within the mitochondria. Experiments with dideoxycytidine revealed that 10-fold decrease of the mtDNA copy number resulted in almost normal activity of cytochrome c oxidase. We found that mtDNA depletion is compensated mostly on the level of RNA metabolism in the mitochondria. Thus, our results are in agreement with the hypothesis that transcription initiation rather than mtDNA copy number is a rate limiting factor for expression of the mitochondrial genome. |
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Authors:
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Janusz Piechota; Roman Szczesny; Kamila Wolanin; Aleksander Chlebowski; Ewa Bartnik |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2006-09-02 |
Journal Detail:
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Title: Acta biochimica Polonica Volume: 53 ISSN: 0001-527X ISO Abbreviation: Acta Biochim. Pol. Publication Date: 2006 |
Date Detail:
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Created Date: 2006-10-10 Completed Date: 2007-03-05 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 14520300R Medline TA: Acta Biochim Pol Country: Poland |
Other Details:
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Languages: eng Pagination: 485-95 Citation Subset: IM |
Affiliation:
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Department of Genetics and Biotechnology, Warsaw University, Warszawa, Poland. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antimetabolites / pharmacology DNA, Mitochondrial / drug effects*, genetics Electron Transport / genetics Electron Transport Complex IV / genetics Ethidium / pharmacology* Gene Expression / drug effects* Hela Cells Humans Mitochondria / drug effects, genetics, metabolism Mitochondrial Proteins / biosynthesis Nuclear Proteins* Nuclear Respiratory Factor 1 / genetics Oxidative Phosphorylation / drug effects RNA / drug effects, genetics Rats Thiamphenicol / pharmacology* Zalcitabine / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Antimetabolites; 0/DNA, Mitochondrial; 0/Mitochondrial Proteins; 0/Nuclear Proteins; 0/Nuclear Respiratory Factor 1; 0/RNA, mitochondrial; 15318-45-3/Thiamphenicol; 3546-21-2/Ethidium; 63231-63-0/RNA; 7481-89-2/Zalcitabine; EC 1.9.3.1/Electron Transport Complex IV |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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