Evidence map›Paper›PMID 26159996›Full record

ArticleGenes & development2015

H3K36 methylation promotes longevity by enhancing transcriptional fidelity.

Payel Sen, Weiwei Dang, Greg Donahue, Junbiao Dai, Jean Dorsey, Xiaohua Cao, Wei Liu, Kajia Cao, Rocco Perry, Jun Yeop Lee and 10 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing 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

142 citing papers in PubMed, 232 citations in OpenAlex.

  1. Review
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  11. mRNA Isoforms and Variants in Health and Disease.International journal of molecular sciences · 2025
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82 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

20 authors at 5 institutions in 1 country.

Payel SenDepartment of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Weiwei DangDepartment of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; Huffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030, USA;
Greg DonahueDepartment of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Junbiao DaiHigh-Throughput Biology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA;
Jean DorseyDepartment of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Xiaohua CaoHuffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030, USA;
Wei LiuHigh-Throughput Biology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA;
Kajia CaoDepartment of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Rocco PerryDepartment of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Jun Yeop LeeDepartment of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Brian M WaskoDepartment of Pathology, University of Washington, Seattle, Washington 98195, USA;
Daniel T CarrDepartment of Pathology, University of Washington, Seattle, Washington 98195, USA;
Chong HeThe Buck Institute of Research on Aging, Novato, California 94945, USA;
Brett RobisonThe Buck Institute of Research on Aging, Novato, California 94945, USA;
John WagnerDepartment of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Brian D GregoryDepartment of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
Matt KaeberleinDepartment of Pathology, University of Washington, Seattle, Washington 98195, USA;
Brian K KennedyThe Buck Institute of Research on Aging, Novato, California 94945, USA;
Jef D BoekeHigh-Throughput Biology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA; Institute for Systems Genetics, New York University Langone Medical Center, New York, New York 10016, USA.
Shelley L BergerDepartment of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
University of Pennsylvania · USBuck Institute for Research on Aging · USJohns Hopkins University · USUniversity of Washington · USBaylor College of Medicine · US

Funding

SPECIFICITY OF OXYGEN DNA DAMAGE AND MUTAGENESISP01AG001751 · NIA · UNIVERSITY OF WASHINGTON · PI CAMPBELL, MATTHEW D · 1985 to 2021
$29.6M
STRUCTURAL BASIS FOR EPIGENETICS IN AGING AND LONGEVITYP01AG031862 · NIA · WISTAR INSTITUTE · PI GARCIA, BENJAMIN A · 2008 to 2022
$28.3M
University of Washington Nathan Shock Center of Excellence in the Basic Biology of AgingP30AG013280 · NIA · UNIVERSITY OF WASHINGTON · PI Su-In Lee · 1995 to 2026
$27.1M
Environmetal Pathology/Toxicology Training ProgramT32ES007032 · NIEHS · UNIVERSITY OF WASHINGTON · PI FAUSTMAN, ELAINE M, ROSENFELD, MICHAEL E · 1985 to 2023
$10.7M
System approaches to determine mechanisms underlying yeast replicative agingR01AG043080 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI KENNEDY, BRIAN K · 2012 to 2016
$3.0M
Defining the Mechanisms of genotype-dependent responses to caloric restrictionR01AG039390 · NIA · UNIVERSITY OF WASHINGTON · PI KAEBERLEIN, MATT · 2011 to 2015
$1.5M
Regulation of yeast cellular aging through chromatin and novel pathwaysR00AG037646 · NIA · BAYLOR COLLEGE OF MEDICINE · PI DANG, WEIWEI · 2013 to 2015
$740k
Regulation of yeast cellular aging through chromatin and novel pathwaysK99AG037646 · NIA · UNIVERSITY OF PENNSYLVANIA · PI DANG, WEIWEI · 2010 to 2011
$193k
NIA NIH HHS K99/R00AG037646NIA NIH HHS P01 AG001751NIA NIH HHS P01 AG031862NIA NIH HHS P01AG031862NIA NIH HHS P30 AG013280NIA NIH HHS P30AG013280NIA NIH HHS R00 AG037646NIA NIH HHS R01 AG039390NIA NIH HHS R01AG039390NIA NIH HHS R01 AG043080NIA NIH HHS R01AG043080NIEHS NIH HHS T32 ES007032NIEHS NIH HHS T32ES007032NIGMS NIH HHS U54GM103250
6 · The paper itself

Abstract

Epigenetic mechanisms, including histone post-translational modifications, control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging phenomenon of shortened life span, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a life span screen in Saccharomyces cerevisiae that is designed to identify amino acid residues of histones that regulate yeast replicative aging. Our results reveal that lack of sustained histone H3K36 methylation is commensurate with increased cryptic transcription in a subset of genes in old cells and with shorter life span. In contrast, deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes, suppresses cryptic transcript initiation, and extends life span. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to loss of transcriptional precision that is detrimental to life span, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity.

Indexed as

AnimalsCaenorhabditis elegansEpigenesis, GeneticGene DeletionGene Expression Regulation, DevelopmentalHistone DemethylasesHistonesLongevityMethylationMutationProtein Processing, Post-TranslationalRepressor ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsHistone DemethylasesHistonesRepressor ProteinsRPH1 protein, S cerevisiaeSaccharomyces cerevisiae Proteinsagingcryptic transcriptionepigeneticsH3K36 methylation

Identifiers

PMID26159996
PMCPMC4511212
OpenAlexW1956693522

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.