Evidence map›Paper›PMID 31136569›Full record

ArticlePLoS genetics2019

Genetic analyses led to the discovery of a super-active mutant of the RNA polymerase I.

Tommy Darrière, Michael Pilsl, Marie-Kerguelen Sarthou, Adrien Chauvier, Titouan Genty, Sylvain Audibert, Christophe Dez, Isabelle Léger-Silvestre, Christophe Normand, Anthony K Henras and 5 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Cryo-EM structures of human RNA polymerase I.Nature structural & molecular biology · 2021
    Article
  10. Review
  11. Editorial: The Lesser Known World of RNA Polymerases.Frontiers in molecular biosciences · 2021
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. 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

15 authors at 4 institutions in 4 countries.

Tommy DarrièreLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0002-1655-525X
Michael PilslUniversität Regensburg, Biochemie-Zentrum Regensburg (BZR), Lehrstuhl Biochemie III, Regensburg, Germany.
Marie-Kerguelen SarthouLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.
Adrien ChauvierLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0003-4473-6194
Titouan GentyLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.
Sylvain AudibertLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0002-4414-1345
Christophe DezLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0002-8526-3541
Isabelle Léger-SilvestreLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0002-7030-5593
Christophe NormandLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0001-6104-1285
Anthony K HenrasLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.
Marta KwapiszLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.
Olga CalvoInstituto de Biología Funcional y Genómica, IBFG-CSIC, Universidad de Salamanca, Salamanca, Spain.ORCID 0000-0002-9786-7916
Carlos Fernández-TorneroCentro de Investigaciones Biológicas, CSIC, Madrid, Spain.ORCID 0000-0001-5097-731X
Herbert TschochnerUniversität Regensburg, Biochemie-Zentrum Regensburg (BZR), Lehrstuhl Biochemie III, Regensburg, Germany.ORCID 0000-0002-3560-861X
Olivier GadalLaboratoire de Biologie Moléculaire Eucaryote, Centre de Biologie Intégrative (CBI), Université de Toulouse, CNRS, UPS, Toulouse, France.ORCID 0000-0001-9421-0831
Centre National de la Recherche Scientifique · FRUniversity of Regensburg · DECentro de Investigaciones Biológicas Margarita Salas · ESUniversidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Most transcriptional activity of exponentially growing cells is carried out by the RNA Polymerase I (Pol I), which produces a ribosomal RNA (rRNA) precursor. In budding yeast, Pol I is a multimeric enzyme with 14 subunits. Among them, Rpa49 forms with Rpa34 a Pol I-specific heterodimer (homologous to PAF53/CAST heterodimer in human Pol I), which might be responsible for the specific functions of the Pol I. Previous studies provided insight in the involvement of Rpa49 in initiation, elongation, docking and releasing of Rrn3, an essential Pol I transcription factor. Here, we took advantage of the spontaneous occurrence of extragenic suppressors of the growth defect of the rpa49 null mutant to better understand the activity of Pol I. Combining genetic approaches, biochemical analysis of rRNA synthesis and investigation of the transcription rate at the individual gene scale, we characterized mutated residues of the Pol I as novel extragenic suppressors of the growth defect caused by the absence of Rpa49. When mapped on the Pol I structure, most of these mutations cluster within the jaw-lobe module, at an interface formed by the lobe in Rpa135 and the jaw made up of regions of Rpa190 and Rpa12. In vivo, the suppressor allele RPA135-F301S restores normal rRNA synthesis and increases Pol I density on rDNA genes when Rpa49 is absent. Growth of the Rpa135-F301S mutant is impaired when combined with exosome mutation rrp6Δ and it massively accumulates pre-rRNA. Moreover, Pol I bearing Rpa135-F301S is a hyper-active RNA polymerase in an in vitro tailed-template assay. We conclude that RNA polymerase I can be engineered to produce more rRNA in vivo and in vitro. We propose that the mutated area undergoes a conformational change that supports the DNA insertion into the cleft of the enzyme resulting in a super-active form of Pol I.

Indexed as

DNA, RibosomalPol1 Transcription Initiation Complex ProteinsRibosomesRNA Polymerase IRNA PrecursorsRNA, RibosomalSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsTranscription, GeneticDNA, RibosomalPol1 Transcription Initiation Complex ProteinsRNA Polymerase IRNA PrecursorsRNA, RibosomalSaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

PMID31136569
PMCPMC6555540
OpenAlexW2945141847

What OpenQuestion holds

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LicenceCC BY
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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.