Evidence map›Paper›PMID 26300265›Full record

ArticleMolecular cell2015

Global Promoter Targeting of a Conserved Lysine Deacetylase for Transcriptional Shutoff during Quiescence Entry.

Jeffrey N McKnight, Joseph W Boerma, Linda L Breeden, Toshio Tsukiyama

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
5.9field-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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  7. Review
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  14. Cytoophidium complexes resonate with cell fates.Cellular and molecular life sciences : CMLS · 2025
    Article
  15. Stage-specific MCM protein expression inFrontiers in cellular and infection microbiology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Histone deacetylation and cytosine methylation compartmentalize heterochromatic regions in the genome organization ofProceedings of the National Academy of Sciences of the United States of America · 2023
    Article

19 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

4 authors at 1 institution in 1 country.

Jeffrey N McKnightBasic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Joseph W BoermaBasic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Linda L BreedenBasic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. Electronic address: lbreeden@fredhutch.org.
Toshio TsukiyamaBasic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. Electronic address: ttsukiya@fredhutch.org.
Fred Hutch Cancer Center · US

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
Mechanisms and functions of chromatin regulation for cell-cycle controlR01GM111428 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TSUKIYAMA, TOSHIO · 2015 to 2020
$2.4M
Budding yeast longevityR21AG048595 · NIA · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BREEDEN, LINDA L. · 2014 to 2015
$477k
NCI NIH HHS P30 CA015704NCI NIH HHS P30-CA015704-38NIA NIH HHS R21 AG048595NIA NIH HHS R21-AG048595NIGMS NIH HHS R01 GM111428NIGMS NIH HHS R01GM111428
6 · The paper itself

Abstract

Quiescence is a conserved cell-cycle state characterized by cell-cycle arrest, increased stress resistance, enhanced longevity, and decreased transcriptional, translational, and metabolic output. Although quiescence plays essential roles in cell survival and normal differentiation, the molecular mechanisms leading to this state are not well understood. Here, we determined changes in the transcriptome and chromatin structure of S. cerevisiae upon quiescence entry. Our analyses revealed transcriptional shutoff that is far more robust than previously believed and an unprecedented global chromatin transition, which are tightly correlated. These changes require Rpd3 lysine deacetylase targeting to at least half of gene promoters via quiescence-specific transcription factors including Xbp1 and Stb3. Deletion of RPD3 prevents cells from establishing transcriptional quiescence, leading to defects in quiescence entry and shortening of chronological lifespan. Our results define a molecular mechanism for global reprogramming of transcriptome and chromatin structure for quiescence driven by a highly conserved chromatin regulator.

Indexed as

Cell CycleChromatinGene DeletionGenes, FungalHistone DeacetylasesModels, BiologicalPromoter Regions, GeneticRepressor ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTrans-ActivatorsTranscription, GeneticTranscriptomeChromatinHistone DeacetylasesRepressor ProteinsRPD3 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsStb3 protein, S cerevisiaeTrans-ActivatorsXBP1 protein, S cerevisiae

Identifiers

PMID26300265
PMCPMC4560983
OpenAlexW1784555856

What OpenQuestion holds

Textmetadata
LicenceTDM
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.