Evidence map›Paper›PMID 24445803›Full record

ArticleNucleic acids research2014

The amino terminal extension of mammalian mitochondrial RNA polymerase ensures promoter specific transcription initiation.

Viktor Posse, Emily Hoberg, Anke Dierckx, Saba Shahzad, Camilla Koolmeister, Nils-Göran Larsson, L Marcus Wilhelmsson, B Martin Hällberg, Claes M Gustafsson

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Mechanisms and regulation of human mitochondrial transcription.Nature reviews. Molecular cell biology · 2024
    Review
  6. Review
  7. Article
  8. Article
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  12. Article
  13. Article
  14. Article
  15. Mitochondrial diseases: expanding the diagnosis in the era of genetic testing.Journal of translational genetics and genomics · 2020
    Article
  16. Mechanisms of mammalian mitochondrial transcription.Protein science : a publication of the Protein Society · 2019
    Review
  17. Article
  18. Structural basis of mitochondrial transcription.Nature structural & molecular biology · 2018
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Viktor PosseDepartment of Medical Biochemistry and Cell Biology, University of Gothenburg, PO Box 440, Gothenburg, Sweden, Department of Chemical and Biological Engineering/Physical Chemistry, Chalmers University of Technology, S-41296 Gothenburg, Sweden, Department of Cell and Molecular Biology, Karolinska Institutet, S-171 77 Stockholm, Sweden, Department of Laboratory Medicine, Karolinska Institutet, SE-17177 Stockholm, Sweden, Max Planck Institute for Biology of Ageing, Gleueler Str. 50 a D-50931 Cologne, Germany, Centre for Structural Systems Biology, DESY-Campus, D-22603 Hamburg, Germany and European Molecular Biology Laboratory, Hamburg Unit, 22603 Hamburg, Germany.
Emily Hoberg
Anke Dierckx
Saba Shahzad
Camilla Koolmeister
Nils-Göran Larsson
L Marcus Wilhelmsson
B Martin Hällberg
Claes M Gustafsson
Chalmers University of Technology · SEKarolinska Institutet · SEEuropean Molecular Biology Laboratory · DEUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian mitochondrial transcription is executed by a single subunit mitochondrial RNA polymerase (Polrmt) and its two accessory factors, mitochondrial transcription factors A and B2 (Tfam and Tfb2m). Polrmt is structurally related to single-subunit phage RNA polymerases, but it also contains a unique N-terminal extension (NTE) of unknown function. We here demonstrate that the NTE functions together with Tfam to ensure promoter-specific transcription. When the NTE is deleted, Polrmt can initiate transcription in the absence of Tfam, both from promoters and non-specific DNA sequences. Additionally, when in presence of Tfam and a mitochondrial promoter, the NTE-deleted mutant has an even higher transcription activity than wild-type polymerase, indicating that the NTE functions as an inhibitory domain. Our studies lead to a model according to which Tfam specifically recruits wild-type Polrmt to promoter sequences, relieving the inhibitory effect of the NTE, as a first step in transcription initiation. In the second step, Tfb2m is recruited into the complex and transcription is initiated.

Indexed as

Promoter Regions, GeneticTranscription Initiation, GeneticAnimalsDNA-Binding ProteinsDNA-Directed RNA PolymerasesHigh Mobility Group ProteinsHumansMethyltransferasesMiceMitochondriaMitochondrial ProteinsMutationProtein Structure, TertiaryTranscription FactorsDNA-Binding ProteinsDNA-Directed RNA PolymerasesHigh Mobility Group ProteinsMethyltransferasesMitochondrial ProteinsPOLRMT protein, humanPolrmt protein, mouseTfam protein, mouseTFB2M protein, humanTranscription Factors

Identifiers

PMID24445803
PMCPMC3973307
OpenAlexW1979602987

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.