Evidence map›Paper›PMID 27688402›Full record

ArticleGenes & development2016

E2F coregulates an essential HSF developmental program that is distinct from the heat-shock response.

Jian Li, Laetitia Chauve, Grace Phelps, Renée M Brielmann, Richard I Morimoto

Abstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing 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

81 citing papers in PubMed.

  1. More than the 'master regulator of cytosolic proteostasis': new roles for HSF1 in promoting tissue health.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  2. Regulation of cellular proteostasis via mitochondrial protein import.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  3. Adaptation to heat stress by diversification of the vertebrate heat shock transcription factor family.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
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  7. Review
  8. A default silencing mechanism restrains stress-induced genes inbioRxiv : the preprint server for biology · 2025
    Article
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21 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

5 authors.

Jian LiDepartment of Molecular Biosciences, Rice Institute for Biomedical Research, Northwestern University, Evanston, Illinois 60208, USA.
Laetitia ChauveDepartment of Molecular Biosciences, Rice Institute for Biomedical Research, Northwestern University, Evanston, Illinois 60208, USA.
Grace PhelpsDepartment of Molecular Biosciences, Rice Institute for Biomedical Research, Northwestern University, Evanston, Illinois 60208, USA.
Renée M BrielmannDepartment of Molecular Biosciences, Rice Institute for Biomedical Research, Northwestern University, Evanston, Illinois 60208, USA.
Richard I MorimotoDepartment of Molecular Biosciences, Rice Institute for Biomedical Research, Northwestern University, Evanston, Illinois 60208, USA.

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Tissue resident macrophages regulate proteostasis in the aging lungP01AG049665 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GR Scott Budinger · 2015 to 2026
$26.9M
Modeling the temporal succession of phenotypes & environnnental cuesP50MH094267 · NIMH · UNIVERSITY OF CHICAGO · PI RZHETSKY, ANDREY · 2011 to 2015
$10.2M
C. elegans Model for Neurodegenerative Diseases of AgingR37AG026647 · NIA · NORTHWESTERN UNIVERSITY · PI MORIMOTO, RICHARD I · 2010 to 2019
$3.9M
NCI NIH HHS P30 CA060553NIA NIH HHS P01 AG049665NIA NIH HHS R37 AG026647NIMH NIH HHS P50 MH094267
6 · The paper itself

Abstract

Heat-shock factor (HSF) is the master transcriptional regulator of the heat-shock response (HSR) and is essential for stress resilience. HSF is also required for metazoan development; however, its function and regulation in this process are poorly understood. Here, we characterize the genomic distribution and transcriptional activity of Caenorhabditis elegans HSF-1 during larval development and show that the developmental HSF-1 transcriptional program is distinct from the HSR. HSF-1 developmental activation requires binding of E2F/DP to a GC-rich motif that facilitates HSF-1 binding to a heat-shock element (HSE) that is degenerate from the consensus HSE sequence and adjacent to the E2F-binding site at promoters. In contrast, induction of the HSR is independent of these promoter elements or E2F/DP and instead requires a distinct set of tandem canonical HSEs. Together, E2F and HSF-1 directly regulate a gene network, including a specific subset of chaperones, to promote protein biogenesis and anabolic metabolism, which are essential in development.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsE2F Transcription FactorsGene Regulatory NetworksGenome, HelminthHeat-Shock ResponseLarvaNucleotide MotifsPromoter Regions, GeneticProtein BindingCaenorhabditis elegans ProteinsE2F Transcription FactorsCaenorhabditis elegansdevelopmentE2F transcription factorheat-shock factor (HSF)molecular chaperonesstress responsetranscription regulation

Identifiers

PMID27688402
PMCPMC5066613

What OpenQuestion holds

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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.