Evidence map›Paper›PMID 27605042›Full record

ArticleScientific reports2016

Loss of Tau protein affects the structure, transcription and repair of neuronal pericentromeric heterochromatin.

Zeyni Mansuroglu, Houda Benhelli-Mokrani, Vasco Marcato, Audrey Sultan, Marie Violet, Alban Chauderlier, Lucie Delattre, Anne Loyens, Smail Talahari, Séverine Bégard and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
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26 more citing papers are in PubMed but not listed here.

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

17 authors at 3 institutions in 1 country.

Zeyni MansurogluUniversité Paris Descartes, Centre Interdisciplinaire Chimie Biologie-Paris, Inserm UMRS1007, Paris, France.
Houda Benhelli-MokraniUniversité Paris Descartes, Centre Interdisciplinaire Chimie Biologie-Paris, Inserm UMRS1007, Paris, France.
Vasco MarcatoUniversité Paris Descartes, Centre Interdisciplinaire Chimie Biologie-Paris, Inserm UMRS1007, Paris, France.
Audrey SultanUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Marie VioletUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Alban ChauderlierUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Lucie DelattreUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Anne LoyensUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Smail TalahariLaboratoire de Toxicologie Génétique, Institut Pasteur de Lille, Lille, France.
Séverine BégardUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Fabrice NesslanyLaboratoire de Toxicologie Génétique, Institut Pasteur de Lille, Lille, France.
Morvane ColinUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Sylvie SouèsUniversité Paris Descartes, Centre Interdisciplinaire Chimie Biologie-Paris, Inserm UMRS1007, Paris, France.
Bruno LefebvreUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Luc BuéeUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Marie-Christine GalasUniversité de Lille, Inserm, CHU-Lille, UMRS1172, Alzheimer &Tauopathies, Lille, France.
Eliette BonnefoyUniversité Paris Descartes, Centre Interdisciplinaire Chimie Biologie-Paris, Inserm UMRS1007, Paris, France.
Inserm · FRInstitut Pasteur de Lille · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pericentromeric heterochromatin (PCH) gives rise to highly dense chromatin sub-structures rich in the epigenetic mark corresponding to the trimethylated form of lysine 9 of histone H3 (H3K9me3) and in heterochromatin protein 1α (HP1α), which regulate genome expression and stability. We demonstrate that Tau, a protein involved in a number of neurodegenerative diseases including Alzheimer's disease (AD), binds to and localizes within or next to neuronal PCH in primary neuronal cultures from wild-type mice. Concomitantly, we show that the clustered distribution of H3K9me3 and HP1α, two hallmarks of PCH, is disrupted in neurons from Tau-deficient mice (KOTau). Such altered distribution of H3K9me3 that could be rescued by overexpressing nuclear Tau protein was also observed in neurons from AD brains. Moreover, the expression of PCH non-coding RNAs, involved in PCH organization, was disrupted in KOTau neurons that displayed an abnormal accumulation of stress-induced PCH DNA breaks. Altogether, our results demonstrate a new physiological function of Tau in directly regulating neuronal PCH integrity that appears disrupted in AD neurons.

Indexed as

AnimalsBrainCentromereChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDNA BreaksDNA RepairEpigenesis, GeneticHeterochromatinHistonesHumansLysineMiceMice, KnockoutNeuronstau ProteinsCBX5 protein, humanChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHeterochromatinHistonesLysinetau Proteins

Identifiers

PMID27605042
PMCPMC5015075
OpenAlexW2514975062

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.