Evidence map›Paper›PMID 30894545›Full record

ArticleNature communications2019

Functional interplay between TFIIH and KAT2A regulates higher-order chromatin structure and class II gene expression.

Jérémy Sandoz, Zita Nagy, Philippe Catez, Gizem Caliskan, Sylvain Geny, Jean-Baptiste Renaud, Jean-Paul Concordet, Arnaud Poterszman, Laszlo Tora, Jean-Marc Egly and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-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

14 citing papers in PubMed, 14 citations in OpenAlex.

  1. Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026
    Review
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  8. Genes · 2022
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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

12 authors at 2 institutions in 1 country.

Jérémy SandozInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France.
Zita NagyInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France.
Philippe CatezInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France.
Gizem CaliskanInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France.
Sylvain GenyLaboratoire Structure et Instabilité des Génomes, INSERM U1154, CNRS UMR7196, Muséum national d'Histoire naturelle, 43 rue Cuvier, 75005, Paris, France.
Jean-Baptiste RenaudLaboratoire Structure et Instabilité des Génomes, INSERM U1154, CNRS UMR7196, Muséum national d'Histoire naturelle, 43 rue Cuvier, 75005, Paris, France.
Jean-Paul ConcordetLaboratoire Structure et Instabilité des Génomes, INSERM U1154, CNRS UMR7196, Muséum national d'Histoire naturelle, 43 rue Cuvier, 75005, Paris, France.
Arnaud PoterszmanInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France.
Laszlo ToraInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France.ORCID http://orcid.org/0000-0001-7398-2250
Jean-Marc EglyInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France.
Nicolas Le MayInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France.
Frédéric CoinInstitut de Génétique et de Biologie Moléculaire et Cellulaire Illkirch Cedex, C.U. Strasbourg, France. fredr@igbmc.fr.
Centre National de la Recherche Scientifique · FRInstitut de génétique et de biologie moléculaire et cellulaire · FR

Funding

European Research Council 340551
6 · The paper itself

Abstract

The TFIIH subunit XPB is involved in combined Xeroderma Pigmentosum and Cockayne syndrome (XP-B/CS). Our analyses reveal that XPB interacts functionally with KAT2A, a histone acetyltransferase (HAT) that belongs to the hSAGA and hATAC complexes. XPB interacts with KAT2A-containing complexes on chromatin and an XP-B/CS mutation specifically elicits KAT2A-mediated large-scale chromatin decondensation. In XP-B/CS cells, the abnormal recruitment of TFIIH and KAT2A to chromatin causes inappropriate acetylation of histone H3K9, leading to aberrant formation of transcription initiation complexes on the promoters of several hundred genes and their subsequent overexpression. Significantly, this cascade of events is similarly sensitive to KAT2A HAT inhibition or to the rescue with wild-type XPB. In agreement, the XP-B/CS mutation increases KAT2A HAT activity in vitro. Our results unveil a tight connection between TFIIH and KAT2A that controls higher-order chromatin structure and gene expression and provide new insights into transcriptional misregulation in a cancer-prone DNA repair-deficient disorder.

Indexed as

AcetylationCell Line, TumorChromatinCockayne SyndromeCRISPR-Associated Protein 9CRISPR-Cas SystemsFibroblastsGene EditingGene Expression RegulationHistone AcetyltransferasesHistonesHumansModels, BiologicalOsteoblastsp300-CBP-Associated FactorPrimary Cell CultureChromatinCRISPR-Associated Protein 9Histone AcetyltransferasesHistonesKAT2A protein, humanp300-CBP-Associated FactorProtein SubunitsRNA, Guide, CRISPR-Cas SystemsRNA, Small InterferingTranscription Factor TFIIH

Identifiers

PMID30894545
PMCPMC6426930
OpenAlexW2924047243

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.