Evidence map›Paper›PMID 34722523›Full record

ArticleFrontiers in cell and developmental biology2021

Tau Stabilizes Chromatin Compaction.

Thomas Rico, Melissa Gilles, Alban Chauderlier, Thomas Comptdaer, Romain Magnez, Maggy Chwastyniak, Herve Drobecq, Florence Pinet, Xavier Thuru, Luc Buée and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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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 6 institutions in 1 country.

Thomas RicoUniv. Lille, INSERM, CHU-Lille, Lille Neuroscience and Cognition, UMR-S1172, Alzheimer and Tauopathies, Lille, France.
Melissa GillesUniv. Lille, INSERM, CHU-Lille, Lille Neuroscience and Cognition, UMR-S1172, Alzheimer and Tauopathies, Lille, France.
Alban ChauderlierUniv. Lille, INSERM, CHU-Lille, Lille Neuroscience and Cognition, UMR-S1172, Alzheimer and Tauopathies, Lille, France.
Thomas ComptdaerUniv. Lille, INSERM, CHU-Lille, Lille Neuroscience and Cognition, UMR-S1172, Alzheimer and Tauopathies, Lille, France.
Romain MagnezUniv. Lille, CNRS, INSERM, CHU Lille, UMR 9020, UMR 1277, Canther, Platform of Integrative Chemical Biology, Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France.
Maggy ChwastyniakUniv. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167 - RID-AGE - Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, Lille, France.
Herve DrobecqUniv. Lille, CNRS UMR 9017, INSERM U1019, CHRU Lille, Institut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Florence PinetUniv. Lille, INSERM, CHU Lille, Institut Pasteur de Lille, U1167 - RID-AGE - Facteurs de Risque et Déterminants Moléculaires des Maladies Liées Au Vieillissement, Lille, France.
Xavier ThuruUniv. Lille, CNRS, INSERM, CHU Lille, UMR 9020, UMR 1277, Canther, Platform of Integrative Chemical Biology, Cancer Heterogeneity, Plasticity and Resistance to Therapies, Lille, France.
Luc BuéeUniv. Lille, INSERM, CHU-Lille, Lille Neuroscience and Cognition, UMR-S1172, Alzheimer and Tauopathies, Lille, France.
Marie-Christine GalasUniv. Lille, INSERM, CHU-Lille, Lille Neuroscience and Cognition, UMR-S1172, Alzheimer and Tauopathies, Lille, France.
Bruno LefebvreUniv. Lille, INSERM, CHU-Lille, Lille Neuroscience and Cognition, UMR-S1172, Alzheimer and Tauopathies, Lille, France.
Centre de Recherche Jean Pierre Aubert · FRCentre National de la Recherche Scientifique · FRInserm · FRInstitut Pasteur de Lille · FRLille Neurosciences & CognitionUniversité de Lille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An extensive body of literature suggested a possible role of the microtubule-associated protein Tau in chromatin functions and/or organization in neuronal, non-neuronal, and cancer cells. How Tau functions in these processes remains elusive. Here we report that Tau expression in breast cancer cell lines causes resistance to the anti-cancer effects of histone deacetylase inhibitors, by preventing histone deacetylase inhibitor-inducible gene expression and remodeling of chromatin structure. We identify Tau as a protein recognizing and binding to core histone when H3 and H4 are devoid of any post-translational modifications or acetylated H4 that increases the Tau's affinity. Consistent with chromatin structure alterations in neurons found in frontotemporal lobar degeneration, Tau mutations did not prevent histone deacetylase-inhibitor-induced higher chromatin structure remodeling by suppressing Tau binding to histones. In addition, we demonstrate that the interaction between Tau and histones prevents further histone H3 post-translational modifications induced by histone deacetylase-inhibitor treatment by maintaining a more compact chromatin structure. Altogether, these results highlight a new cellular role for Tau as a chromatin reader, which opens new therapeutic avenues to exploit Tau biology in neuronal and cancer cells.

Indexed as

cancer biologychromatin regulationchromatin remodelinghistone deacetylase inhibitor (HDAC inhibitor)histone (de)acetylationhistone modification and chromatin structureTau protein (Tau)

Identifiers

PMID34722523
PMCPMC8551707
OpenAlexW3205310051

What OpenQuestion holds

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LicenceCC BY
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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.