Evidence map›Paper›PMID 19008953›Full record

ArticlePLoS genetics2008

p8/TTDA overexpression enhances UV-irradiation resistance and suppresses TFIIH mutations in a Drosophila trichothiodystrophy model.

Javier Aguilar-Fuentes, Mariana Fregoso, Mariana Herrera, Enrique Reynaud, Cathy Braun, Jean Marc Egly, Mario Zurita

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

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  7. The essential and multifunctional TFIIH complex.Protein science : a publication of the Protein Society · 2018
    Review
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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

7 authors at 2 institutions in 2 countries.

Javier Aguilar-FuentesDepartment of Developmental Genetics, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Mexico.
Mariana Fregoso
Mariana Herrera
Enrique Reynaud
Cathy Braun
Jean Marc Egly
Mario Zurita
Universidad Nacional Autónoma de México · MXInstitut de Biologie Moléculaire et Cellulaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in certain subunits of the DNA repair/transcription factor complex TFIIH are linked to the human syndromes xeroderma pigmentosum (XP), Cockayne's syndrome (CS), and trichothiodystrophy (TTD). One of these subunits, p8/TTDA, interacts with p52 and XPD and is important in maintaining TFIIH stability. Drosophila mutants in the p52 (Dmp52) subunit exhibit phenotypic defects similar to those observed in TTD patients with defects in p8/TTDA and XPD, including reduced levels of TFIIH. Here, we demonstrate that several Dmp52 phenotypes, including lethality, developmental defects, and sterility, can be suppressed by p8/TTDA overexpression. TFIIH levels were also recovered in rescued flies. In addition, p8/TTDA overexpression suppressed a lethal allele of the Drosophila XPB homolog. Furthermore, transgenic flies overexpressing p8/TTDA were more resistant to UV irradiation than were wild-type flies, apparently because of enhanced efficiency of cyclobutane-pyrimidine-dimers and 6-4 pyrimidine-pyrimidone photoproducts repair. This study is the first using an intact higher-animal model to show that one subunit mutant can trans-complement another subunit in a multi-subunit complex linked to human diseases.

Indexed as

Gene ExpressionSuppression, GeneticAnimalsDisease Models, AnimalDown-RegulationDrosophilaDrosophila ProteinsHumansProtein SubunitsRadiation ToleranceTranscription Factor TFIIHTrichothiodystrophy SyndromesUltraviolet RaysDrosophila Proteinsmrn protein, DrosophilaProtein SubunitsTranscription Factor TFIIH

Identifiers

PMID19008953
PMCPMC2576456
OpenAlexW2050730782

What OpenQuestion holds

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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.