Evidence map›Paper›PMID 38977420›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2024

Histone H3.3 chaperone HIRA renders stress-responsive genes poised for prospective lethal stresses in acquired tolerance.

Yoshikazu Nagagaki, Yuji Kozakura, Theventhiran Mahandaran, Yukiko Fumoto, Ryuichiro Nakato, Katsuhiko Shirahige, Fuyuki Ishikawa

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2024. 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
–field-weighted citation impact
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.

  1. Article
  2. 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

7 authors.

Yoshikazu NagagakiDepartment of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0009-0005-7865-1158
Yuji KozakuraDepartment of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
Theventhiran MahandaranDepartment of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-7874-7687
Yukiko FumotoDepartment of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
Ryuichiro NakatoLaboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.
Katsuhiko ShirahigeLaboratory of Genome Structure and Function, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.
Fuyuki IshikawaDepartment of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.ORCID https://orcid.org/0000-0002-5580-2305

Funding

Japan Agency for Medical Research and Development 21cm0106113h0006Japan Society for the Promotion of Science 14J08310Japan Society for the Promotion of Science 15H02383Japan Society for the Promotion of Science 25134710Japan Society for the Promotion of Science JPJSCCA20200009Uehara Memorial Foundation 202220433
6 · The paper itself

Abstract

Appropriate responses to environmental challenges are imperative for the survival of all living organisms. Exposure to low-dose stresses is recognized to yield increased cellular fitness, a phenomenon termed hormesis. However, our molecular understanding of how cells respond to low-dose stress remains profoundly limited. Here we report that histone variant H3.3-specific chaperone, HIRA, is required for acquired tolerance, where low-dose heat stress exposure confers resistance to subsequent lethal heat stress. We found that human HIRA activates stress-responsive genes, including HSP70, by depositing histone H3.3 following low-dose stresses. These genes are also marked with histone H3 Lys-4 trimethylation and H3 Lys-9 acetylation, both active chromatin markers. Moreover, depletion of HIRA greatly diminished acquired tolerance, both in normal diploid fibroblasts and in HeLa cells. Collectively, our study revealed that HIRA is required for eliciting adaptive stress responses under environmental fluctuations and is a master regulator of stress tolerance.

Indexed as

Cell Cycle ProteinsHeat-Shock ResponseHistone ChaperonesHistonesTranscription FactorsAcetylationAdaptation, PhysiologicalFibroblastsHeLa CellsHSP70 Heat-Shock ProteinsHumansStress, PhysiologicalCell Cycle ProteinsHIRA protein, humanHistone ChaperonesHistonesHSP70 Heat-Shock ProteinsTranscription Factorsacquired toleranceChromatin remodelingheat shock proteinHIRAhistone chaperonehistone H3.3hormesisstress response

Identifiers

PMID38977420
PMCPMC11447927

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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.