Evidence map›Paper›PMID 28947735›Full record

ArticleNature communications2017

A role for Tau protein in maintaining ribosomal DNA stability and cytidine deaminase-deficient cell survival.

Elias Bou Samra, Géraldine Buhagiar-Labarchède, Christelle Machon, Jérôme Guitton, Rosine Onclercq-Delic, Michael R Green, Olivier Alibert, Claude Gazin, Xavier Veaute, Mounira Amor-Guéret

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  7. Nuclear face of Tau: an inside player in neurodegeneration.Acta neuropathologica communications · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Tau Stabilizes Chromatin Compaction.Frontiers in cell and developmental biology · 2021
    Article
  13. Review
  14. Article
  15. Article
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  17. 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

10 authors at 4 institutions in 2 countries.

Elias Bou SamraInstitut Curie, PSL Research University, UMR 3348, Orsay, 91405, France.
Géraldine Buhagiar-LabarchèdeInstitut Curie, PSL Research University, UMR 3348, Orsay, 91405, France.ORCID http://orcid.org/0000-0002-2282-6693
Christelle MachonLaboratoire de Biochimie et Toxicologie, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, Pierre-Bénite, 69495, France.
Jérôme GuittonLaboratoire de Biochimie et Toxicologie, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, Pierre-Bénite, 69495, France.
Rosine Onclercq-DelicInstitut Curie, PSL Research University, UMR 3348, Orsay, 91405, France.ORCID http://orcid.org/0000-0001-7376-1095
Michael R GreenHoward Hughes Medical Institute, University of Massachusetts Medical School, Worcester, Massachusetts, 01605, USA.ORCID http://orcid.org/0000-0003-3017-3298
Olivier AlibertCEA-DRF-iRCM-LEFG-Genopole, Evry, 91057, France.ORCID http://orcid.org/0000-0002-2686-2034
Claude GazinCEA-DRF-iRCM-LEFG-Genopole, Evry, 91057, France.
Xavier VeauteCEA-DRF-iRCM-CIGEx, Fontenay-aux-Roses, 92265, France.ORCID http://orcid.org/0000-0003-4868-247X
Mounira Amor-GuéretInstitut Curie, PSL Research University, UMR 3348, Orsay, 91405, France. mounira.amor@curie.fr.ORCID http://orcid.org/0000-0002-7713-167X
Université Paris-Sud · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRUniversité Claude Bernard Lyon 1 · FRHoward Hughes Medical Institute · US

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Cells from Bloom's syndrome patients display genome instability due to a defective BLM and the downregulation of cytidine deaminase. Here, we use a genome-wide RNAi-synthetic lethal screen and transcriptomic profiling to identify genes enabling BLM-deficient and/or cytidine deaminase-deficient cells to tolerate constitutive DNA damage and replication stress. We found a synthetic lethal interaction between cytidine deaminase and microtubule-associated protein Tau deficiencies. Tau is overexpressed in cytidine deaminase-deficient cells, and its depletion worsens genome instability, compromising cell survival. Tau is recruited, along with upstream-binding factor, to ribosomal DNA loci. Tau downregulation decreases upstream binding factor recruitment, ribosomal RNA synthesis, ribonucleotide levels, and affects ribosomal DNA stability, leading to the formation of a new subclass of human ribosomal ultrafine anaphase bridges. We describe here Tau functions in maintaining survival of cytidine deaminase-deficient cells, and ribosomal DNA transcription and stability. Moreover, our findings for cancer tissues presenting concomitant cytidine deaminase underexpression and Tau upregulation open up new possibilities for anti-cancer treatment.Cytidine deaminase (CDA) deficiency leads to genome instability. Here the authors find a synthetic lethal interaction between CDA and the microtubule-associated protein Tau deficiencies, and report that Tau depletion affects rRNA synthesis, ribonucleotide pool balance, and rDNA stability.

Indexed as

Bloom SyndromeCell SurvivalCytidine DeaminaseDNA, RibosomalDown-RegulationGenomic InstabilityHeLa CellsHumansRecQ Helicasestau ProteinsUp-RegulationBloom syndrome proteinCytidine DeaminaseDNA, RibosomalRecQ Helicasestau Proteins

Identifiers

PMID28947735
PMCPMC5612969
OpenAlexW2756095359

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.