Evidence map›Paper›PMID 24661334›Full record

ArticleMolecular microbiology2014

Nucleotide excision repair in Trypanosoma brucei: specialization of transcription-coupled repair due to multigenic transcription.

Carlos R Machado, João P Vieira-da-Rocha, Isabela Cecilia Mendes, Matheus A Rajão, Lucio Marcello, Mainá Bitar, Marcela G Drummond, Priscila Grynberg, Denise A A Oliveira, Catarina Marques and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Relationship betweenMedicina (Kaunas, Lithuania) · 2024
    Pooled it
  2. Review
  3. Article
  4. RAD51-mediated R-loop formation acts to repair transcription-associated DNA breaks driving antigenic variation inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Unpicking the Roles of DNA Damage Protein Kinases in Trypanosomatids.Frontiers in cell and developmental biology · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. 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

12 authors at 4 institutions in 3 countries.

Carlos R MachadoDepartamento de Bioquímica e Imunologia, ICB, Universidade Federal de Minas Gerais, Av. Antônio Carlos, 6627, Caixa Postal 486, Belo Horizonte, 30161-970, MG, Brazil.
João P Vieira-da-Rocha
Isabela Cecilia Mendes
Matheus A Rajão
Lucio Marcello
Mainá Bitar
Marcela G Drummond
Priscila Grynberg
Denise A A Oliveira
Catarina Marques
Ben Van Houten
Richard McCulloch
Universidade Federal de Minas Gerais · BRUniversity of Glasgow · GBInstituto Nacional do Câncer · BRUPMC Hillman Cancer Center · US

Funding

DNA damage recognition by nucleotide excision repair proteinsR01ES019566 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI VAN HOUTEN, BENNETT · 2011 to 2020
$3.9M
Medical Research Council G0401553NIEHS NIH HHS R01 ES019566Wellcome Trust 083485Wellcome Trust 085349
6 · The paper itself

Abstract

Nucleotide excision repair (NER) is a highly conserved genome repair pathway acting on helix distorting DNA lesions. NER is divided into two subpathways: global genome NER (GG-NER), which is responsible for repair throughout genomes, and transcription-coupled NER (TC-NER), which acts on lesions that impede transcription. The extent of the Trypanosoma brucei genome that is transcribed is highly unusual, since most genes are organized in multigene transcription units, each transcribed from a single promoter. Given this transcription organization, we have addressed the importance of NER to T. brucei genome maintenance by performing RNAi against all predicted contributing factors. Our results indicate that TC-NER is the main pathway of NER repair, but only CSB, XPBz and XPG contribute. Moreover, we show that UV lesions are inefficiently repaired in T. brucei, perhaps due to preferential use of RNA polymerase translesion synthesis. RNAi of XPC and DDB was found to be lethal, and we show that these factors act in inter-strand cross-link repair. XPD and XPB appear only to act in transcription, not repair. This work indicates that the predominance of multigenic transcription in T. brucei has resulted in pronounced adaptation of NER relative to the host and may be an attractive drug target.

Indexed as

DNA RepairTranscription, GeneticDNA Repair EnzymesGenes, EssentialTrypanosoma brucei bruceiDNA Repair Enzymes

Identifiers

PMID24661334
PMCPMC4138998
OpenAlexW2141690385

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.