Evidence map›Paper›PMID 18308726›Full record

ArticleThe Journal of biological chemistry2008

Mitochondrial transcription factor B2 is essential for metabolic function in Drosophila melanogaster development.

Cristina Adán, Yuichi Matsushima, Rosana Hernández-Sierra, Raquel Marco-Ferreres, Miguel Angel Fernández-Moreno, Emiliano González-Vioque, Manuel Calleja, Juan J Aragón, Laurie S Kaguni, Rafael Garesse

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

10 authors at 2 institutions in 2 countries.

Cristina AdánDepartamento de Bioquímica, Instituto de Investigaciones Biomédicas Alberto Sols CSIC-UAM, CIBERER ISCIII, Facultad de Medicina, Universidad Autónoma de Madrid, C/Arzobispo Morcillo 4, E-28029 Madrid, Spain.
Yuichi Matsushima
Rosana Hernández-Sierra
Raquel Marco-Ferreres
Miguel Angel Fernández-Moreno
Emiliano González-Vioque
Manuel Calleja
Juan J Aragón
Laurie S Kaguni
Rafael Garesse
Universidad Autónoma de Madrid · ESMichigan State University · US

Funding

Mitochondrial DNA Replisome: Mechanism, Structure and PhysiologyR01GM045295 · NIGMS · MICHIGAN STATE UNIVERSITY · PI KAGUNI, LAURIE SIMON · 1991 to 2013
$4.0M
NIGMS NIH HHS GM45295
6 · The paper itself

Abstract

Characterization of the basal transcription machinery of mitochondrial DNA (mtDNA) is critical to understand mitochondrial pathophysiology. In mammalian in vitro systems, mtDNA transcription requires mtRNA polymerase, transcription factor A (TFAM), and either transcription factor B1 (TFB1M) or B2 (TFB2M). We have silenced the expression of TFB2M by RNA interference in Drosophila melanogaster. RNA interference knockdown of TF2BM causes lethality by arrest of larval development. Molecular analysis demonstrates that TF2BM is essential for mtDNA transcription during Drosophila development and is not redundant with TFB1M. The impairment of mtDNA transcription causes a dramatic decrease in oxidative phosphorylation and mitochondrial ATP synthesis in the long-lived larvae, and a metabolic shift to glycolysis, which partially restores ATP levels and elicits a compensatory response at the nuclear level that increases mitochondrial mass. At the cellular level, the mitochondrial dysfunction induced by TFB2M knockdown causes a severe reduction in cell proliferation without affecting cell growth, and increases the level of apoptosis. In contrast, cell differentiation and morphogenesis are largely unaffected. Our data demonstrate the essential role of TFB2M in mtDNA transcription in a multicellular organism, and reveal the complex cellular, biochemical, and molecular responses induced by impairment of oxidative phosphorylation during Drosophila development.

Indexed as

Adenosine TriphosphateAnimalsApoptosisBody PatterningBody WeightCell ProliferationDNA, MitochondrialDrosophila melanogasterDrosophila ProteinsEnergy MetabolismGene Expression Regulation, DevelopmentalGene SilencingGlycolysisLarvaLongevityMitochondriaAdenosine TriphosphateDNA, MitochondrialDrosophila ProteinsRNA, Messenger

Identifiers

PMID18308726
PMCPMC2431005
OpenAlexW1996809767

What OpenQuestion holds

Textmetadata
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.