Evidence map›Paper›PMID 19019151›Full record

ArticleMolecular microbiology2008

A new function of Trypanosoma brucei mitochondrial topoisomerase II is to maintain kinetoplast DNA network topology.

Megan E Lindsay, Eva Gluenz, Keith Gull, Paul T Englund

Open access · bronzeAbstract read
In one paragraph

Article in Molecular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Twist and Turn-Topoisomerase Functions in Mitochondrial DNA Maintenance.International journal of molecular sciences · 2019
    Review
  5. Article
  6. Physiological Roles of DNA Double-Strand Breaks.Journal of nucleic acids · 2017
    Review
  7. Article
  8. Article
  9. A passion for parasites.The Journal of biological chemistry · 2014
    Article
  10. Trypanosomatids topoisomerase re-visited. New structural findings and role in drug discovery.International journal for parasitology. Drugs and drug resistance · 2014
    Review
  11. Article
  12. Single point mutations in ATP synthase compensate for mitochondrial genome loss in trypanosomes.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  13. Article
  14. Genomic organization of leishmania species.Iranian journal of parasitology · 2011
    Article
  15. Article
  16. Article
  17. Article
  18. Drosophila topo IIIalpha is required for the maintenance of mitochondrial genome and male germ-line stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2010
    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

4 authors at 3 institutions in 2 countries.

Megan E LindsayDepartment of Biological Chemistry, Johns Hopkins Medical School, Baltimore, MD, USA.
Eva Gluenz
Keith Gull
Paul T Englund
University of Oxford · GBJohns Hopkins University · USMolina Center for Energy and the Environment · US

Funding

STRUCTURE AND SYNTHESIS OF DNAR01AI058613 · NIAID · JOHNS HOPKINS UNIVERSITY · PI JENSEN, ROBERT E · 2004 to 2013
$7.4M
NIAID NIH HHS AI058613NIAID NIH HHS R01 AI058613Wellcome Trust
6 · The paper itself

Abstract

The mitochondrial genome of Trypanosoma brucei, called kinetoplast DNA, is a network of topologically interlocked DNA rings including several thousand minicircles and a few dozen maxicircles. Kinetoplast DNA synthesis involves release of minicircles from the network, replication of the free minicircles and reattachment of the progeny. Here we report a new function of the mitochondrial topoisomerase II (TbTOP2mt). Although traditionally thought to reattach minicircle progeny to the network, here we show that it also mends holes in the network created by minicircle release. Network holes are not observed in wild-type cells, implying that this mending reaction is normally efficient. However, RNAi of TbTOP2mt causes holes to persist and enlarge, leading to network fragmentation. Remarkably, these network fragments remain associated within the mitochondrion, and many appear to be appropriately packed at the local level, even as the overall kinetoplast organization is dramatically altered. The deficiency in mending holes is temporally the earliest observable defect in the complex TbTOP2mt RNAi phenotype.

Indexed as

AnimalsDNA, KinetoplastDNA Topoisomerases, Type IIMetabolic Networks and PathwaysMitochondriaMitochondrial ProteinsRNA InterferenceTrypanosoma brucei bruceiDNA, KinetoplastDNA Topoisomerases, Type IIMitochondrial Proteins

Identifiers

PMID19019151
PMCPMC2993328
OpenAlexW2114021644

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.