Evidence map›Paper›PMID 35802638›Full record

ArticlePloS one2022

A stable XPG protein is required for proper ribosome biogenesis: Insights on the phenotype of combinate Xeroderma Pigmentosum/Cockayne Syndrome patients.

Florent Taupelet, Lise-Marie Donnio, Charlène Magnani, Pierre-Olivier Mari, Giuseppina Giglia-Mari

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

5 authors at 1 institution in 1 country.

Florent TaupeletInstitut NeuroMyoGène-Physiopathologie et Génétique du Neurone et du Muscle, CNRS UMR 5261, INSERM U1315, Faculté de Médecine et de Pharmacie Rockefeller, Université Claude Bernard Lyon 1, Lyon, France.ORCID 0000-0002-2214-1096
Lise-Marie DonnioInstitut NeuroMyoGène-Physiopathologie et Génétique du Neurone et du Muscle, CNRS UMR 5261, INSERM U1315, Faculté de Médecine et de Pharmacie Rockefeller, Université Claude Bernard Lyon 1, Lyon, France.
Charlène MagnaniInstitut NeuroMyoGène-Physiopathologie et Génétique du Neurone et du Muscle, CNRS UMR 5261, INSERM U1315, Faculté de Médecine et de Pharmacie Rockefeller, Université Claude Bernard Lyon 1, Lyon, France.
Pierre-Olivier MariInstitut NeuroMyoGène-Physiopathologie et Génétique du Neurone et du Muscle, CNRS UMR 5261, INSERM U1315, Faculté de Médecine et de Pharmacie Rockefeller, Université Claude Bernard Lyon 1, Lyon, France.
Giuseppina Giglia-MariInstitut NeuroMyoGène-Physiopathologie et Génétique du Neurone et du Muscle, CNRS UMR 5261, INSERM U1315, Faculté de Médecine et de Pharmacie Rockefeller, Université Claude Bernard Lyon 1, Lyon, France.ORCID 0000-0003-2001-1965
Université Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nucleotide Excision Repair is one of the five DNA repair systems. More than 30 proteins are involved in this process, including the seven XP proteins. When mutated, the genes coding for these proteins are provoking the rare disease Xeroderma Pigmentosum, which causes cutaneous defects and a high prevalence of skin cancers in patients. The CSA and CSB proteins are also involved in Nucleotide Excision Repair, and their mutation leads to Cockayne Syndrome, another rare disease, causing dwarfism, neurodegeneration, and ultimately early death, but without high skin cancer incidence. Some mutations of ERCC5, the gene coding for XPG, may give rise to a combined Xeroderma Pigmentosum and Cockayne Syndrome. A defect in Nucleotide Excision Repair alone cannot explain all these phenotypes. XPG has been located in the nucleolus, where ribosome biogenesis happens. This energy-consuming process starts with the transcription of the ribosomal DNA in a long ribosomal RNA, the pre-rRNA 47S, by RNA Polymerase 1. 47S pre-rRNA undergoes several cleavages and modifications to form three mature products: the ribosomal RNAs 18S, 5.8S and 28S. In the cytoplasm, these three products will enter the ribosomes' composition, the producers of protein in our cells. Our work aimed to observe ribosome biogenesis in presence of an unstable XPG protein. By working on Xeroderma Pigmentosum/Cockayne Syndrome cell lines, meaning in the absence of XPG, we uncovered that the binding of UBF, as well as the number of unresolved R-loops, is increased along the ribosomal DNA gene body and flanking regions. Furthermore, ribosomal RNA maturation is impaired, with increased use of alternative pathways of maturation as well as an increase of immature precursors. These defective processes may explain the neurodegeneration observed when the XPG protein is heavily truncated, as ribosomal homeostasis and R-loops resolution are critical for proper neuronal development.

Indexed as

Cockayne SyndromeDNA-Binding ProteinsEndonucleasesNuclear ProteinsTranscription FactorsXeroderma PigmentosumDNA Excision Repair Protein ERCC-5DNA RepairDNA, RibosomalHumansPhenotypeRare DiseasesRibosomesRNA PrecursorsRNA, RibosomalDNA-Binding ProteinsDNA Excision Repair Protein ERCC-5DNA, RibosomalEndonucleasesNuclear ProteinsRNA PrecursorsRNA, RibosomalTranscription Factors

Identifiers

PMID35802638
PMCPMC9269744
OpenAlexW4284965498

What OpenQuestion holds

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Registered trials

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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.