Evidence map›Paper›PMID 26304125›Full record

ArticleThe Journal of biological chemistry2015

Differential Editosome Protein Function between Life Cycle Stages of Trypanosoma brucei.

Suzanne M McDermott, Xuemin Guo, Jason Carnes, Kenneth Stuart

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Deep mutational scanning of the RNase III-like domain inFrontiers in cellular and infection microbiology · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. KRGG1 function in RNA editing inRNA (New York, N.Y.) · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. The Architecture of Trypanosoma brucei editosomes.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

4 authors at 1 institution in 1 country.

Suzanne M McDermottFrom the Center for Infectious Disease Research, formerly known as Seattle Biomedical Research Institute, Seattle, Washington 98109.
Xuemin GuoFrom the Center for Infectious Disease Research, formerly known as Seattle Biomedical Research Institute, Seattle, Washington 98109.
Jason CarnesFrom the Center for Infectious Disease Research, formerly known as Seattle Biomedical Research Institute, Seattle, Washington 98109.
Kenneth StuartFrom the Center for Infectious Disease Research, formerly known as Seattle Biomedical Research Institute, Seattle, Washington 98109 ken.stuart@cidresearch.org.
Center for Infectious Disease Research · US

Funding

MITOCHONDRIAL DNA OF NORMAL AND MUTANT TRYPANOSOMESR01AI014102 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI KENNETH D STUART · 1985 to 2026
$20.9M
NIAID NIH HHS R01 AI014102
6 · The paper itself

Abstract

Uridine insertion and deletion RNA editing generates functional mitochondrial mRNAs in Trypanosoma brucei. The mRNAs are differentially edited in bloodstream form (BF) and procyclic form (PF) life cycle stages, and this correlates with the differential utilization of glycolysis and oxidative phosphorylation between the stages. The mechanism that controls this differential editing is unknown. Editing is catalyzed by multiprotein ∼20S editosomes that contain endonuclease, 3'-terminal uridylyltransferase, exonuclease, and ligase activities. These editosomes also contain KREPB5 and KREPA3 proteins, which have no functional catalytic motifs, but they are essential for parasite viability, editing, and editosome integrity in BF cells. We show here that repression of KREPB5 or KREPA3 is also lethal in PF, but the effects on editosome structure differ from those in BF. In addition, we found that point mutations in KREPB5 or KREPA3 differentially affect cell growth, editosome integrity, and RNA editing between BF and PF stages. These results indicate that the functions of KREPB5 and KREPA3 editosome proteins are adjusted between the life cycle stages. This implies that these proteins are involved in the processes that control differential editing and that the 20S editosomes differ between the life cycle stages.

Indexed as

Life Cycle StagesRNA EditingAmino Acid MotifsAmino Acid SequenceBloodCell LineDrug ResistanceModels, MolecularMolecular Sequence DataMutationProtein Structure, TertiaryProtozoan ProteinsRibonuclease IIITetracyclineTrypanosoma brucei bruceiProtozoan ProteinsRibonuclease IIITetracyclinedevelopmental regulationdifferential editingeditosomemitochondriaprotein complexprotein domainprotein-protein interactionRNA editingTrypanosoma brucei

Identifiers

PMID26304125
PMCPMC4599000
OpenAlexW1840502643

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.