ArticleNucleic acids research2002
Modulation of mitochondrial transcription in response to mtDNA depletion and repletion in HeLa cells.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
58 citing papers in PubMed, 132 citations in OpenAlex.
- Role of LONP1 in human diseases: molecular mechanisms and therapeutic potential.Cellular & molecular biology letters · 2026Review
- Mitochondrial transcription factor A: linking mtDNA maintenance, mitochondrial stress responses, and inflammaging.Frontiers in aging · 2026Review
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- Mitochondrial Deoxyribonucleic Acid Copy Number Elevation As a Predictor for Extended Survival and Favorable Outcomes in High-Grade Brain Tumor Patients: A Malaysian Study.The Eurasian journal of medicine · 2024Article
- Mitochondrial E3 ligase MARCH5 is a safeguard against DNA-PKcs-mediated immune signaling in mitochondria-damaged cells.Cell death & disease · 2023Article
- Let's make it clear: systematic exploration of mitochondrial DNA- and RNA-protein complexes by complexome profiling.Nucleic acids research · 2023Article
- 35 Years of TFAM Research: Old Protein, New Puzzles.Biology · 2023Review
- Integrated transcriptomic and metabolomic analysis reveals the metabolic programming of GM-CSF- and M-CSF- differentiated mouse macrophages.Frontiers in immunology · 2023Article
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- Assessing Mitochondrial DNA Release into the Cytosol and Subsequent Activation of Innate Immune-related Pathways in Mammalian Cells.Current protocols · 2022Article
- Mitochondria as target to inhibit proliferation and induce apoptosis of cancer cells: the effects of doxycycline and gemcitabine.Scientific reports · 2020Article
- Characterization of post-edited cells modified in the TFAM gene by CRISPR/Cas9 technology in the bovine model.PloS one · 2020Article
- Limited predictive value of TFAM in mitochondrial biogenesis.Mitochondrion · 2019Article
- Quantitative proteomics revealed C6orf203/MTRES1 as a factor preventing stress-induced transcription deficiency in human mitochondria.Nucleic acids research · 2019Article
- RAD51C/XRCC3 Facilitates Mitochondrial DNA Replication and Maintains Integrity of the Mitochondrial Genome.Molecular and cellular biology · 2018Article
- Mitochondrial DNA depletion, mitochondrial mutations and high TFAM expression in hepatocellular carcinoma.Oncotarget · 2017Article
- Tetramethylpyrazine blocks TFAM degradation and up-regulates mitochondrial DNA copy number by interacting with TFAM.Bioscience reports · 2017Article
- Article
- Mitochondrial Ribosomal Protein L12 Is Required for POLRMT Stability and Exists as Two Forms Generated by Alternative Proteolysis during Import.The Journal of biological chemistry · 2016Article
- Direct evidence of mitochondrial G-quadruplex DNA by using fluorescent anti-cancer agents.Nucleic acids research · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The steady-state amounts of mitochondrial transcripts and transcription proteins were analyzed during mtDNA depletion and subsequent repletion to gain insight into the regulation of human mitochondrial gene expression. As documented previously, HeLa cells depleted of mtDNA via treatment with ethidium bromide (EB) were found to contain reduced steady-state levels of the mitochondrial transcription factor h-mtTFA. When partially mtDNA-depleted cells were cultured in the absence of EB, h-mtTFA recovered to normal levels at a significantly slower rate than mtDNA. Human mtRNA polymerase exhibited a similar depletion-repletion profile, suggesting that the mitochondrial transcription machinery is coordinately regulated in response to changes in mtDNA copy number. Newly synthesized mitochondrial transcripts were detected early in the recovery phase, despite the fact that mtDNA, h-mtTFA and h-mtRNA polymerase were simultaneously depleted. Although delayed relative to mtDNA, the amounts of h-mtTFA and h-mtRNA polymerase sharply increased during the later stages of the recovery phase, which was accompanied by accelerated rates of transcription and mtDNA replication. Altogether, these data indicate that when mtDNA copy number is low, it is beneficial to prevent accumulation of mitochondrial transcription proteins. In addition, h-mtTFA and h-mtRNA polymerase are either normally present in excess of the amount required for transcription or their activity is up-regulated to ensure continued expression and transcription-dependent replication of the mitochondrial genome during mtDNA-depleted states.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.