Evidence map›Paper›PMID 29462149›Full record

ArticlePLoS genetics2018

The INO80 chromatin remodeler sustains metabolic stability by promoting TOR signaling and regulating histone acetylation.

Sean L Beckwith, Erin K Schwartz, Pablo E García-Nieto, Devin A King, Graeme J Gowans, Ka Man Wong, Tessa L Eckley, Alexander P Paraschuk, Egan L Peltan, Laura R Lee and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. 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
1.4field-weighted citation impact, top 18% 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, 34 citations in OpenAlex.

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  5. Frontiers in epigenetics and epigenomics · 2024
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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 1 institution in 1 country.

Sean L BeckwithDepartment of Biology, Stanford University, Stanford, CA, United States of America.ORCID 0000-0001-6559-1030
Erin K SchwartzDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Pablo E García-NietoDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Devin A KingDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Graeme J GowansDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Ka Man WongDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Tessa L EckleyDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Alexander P ParaschukDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Egan L PeltanDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Laura R LeeDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Wei YaoDepartment of Biology, Stanford University, Stanford, CA, United States of America.
Ashby J MorrisonDepartment of Biology, Stanford University, Stanford, CA, United States of America.ORCID 0000-0003-1228-5093
Stanford University · US

Funding

INSTITUTIONAL TRAINING GRANT IN GENOME SCIENCET32HG000044 · NHGRI · STANFORD UNIVERSITY · PI MICHAEL P. SNYDER · 1995 to 2026
$32.2M
Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
The Role of Chromatin in Metabolic Homeostasis SupplementalR35GM119580 · NIGMS · STANFORD UNIVERSITY · PI MORRISON, ASHBY J. · 2016 to 2025
$4.7M
NCI NIH HHS T32 CA009302NHGRI NIH HHS T32 HG000044NIGMS NIH HHS R35 GM119580
6 · The paper itself

Abstract

Chromatin remodeling complexes are essential for gene expression programs that coordinate cell function with metabolic status. However, how these remodelers are integrated in metabolic stability pathways is not well known. Here, we report an expansive genetic screen with chromatin remodelers and metabolic regulators in Saccharomyces cerevisiae. We found that, unlike the SWR1 remodeler, the INO80 chromatin remodeling complex is composed of multiple distinct functional subunit modules. We identified a strikingly divergent genetic signature for the Ies6 subunit module that links the INO80 complex to metabolic homeostasis. In particular, mitochondrial maintenance is disrupted in ies6 mutants. INO80 is also needed to communicate TORC1-mediated signaling to chromatin, as ino80 mutants exhibit defective transcriptional profiles and altered histone acetylation of TORC1-responsive genes. Furthermore, comparative analysis reveals subunits of INO80 and mTORC1 have high co-occurrence of alterations in human cancers. Collectively, these results demonstrate that the INO80 complex is a central component of metabolic homeostasis that influences histone acetylation and may contribute to disease when disrupted.

Indexed as

AcetylationChromatin Assembly and DisassemblyGene Expression Regulation, FungalGenomic InstabilityHistone AcetyltransferasesHistonesHomeostasisMetabolic Networks and PathwaysOrganisms, Genetically ModifiedProtein Processing, Post-TranslationalProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsHistone AcetyltransferasesHistonesINO80 complex, S cerevisiaeProtein Serine-Threonine KinasesSaccharomyces cerevisiae Proteinstarget of rapamycin protein, S cerevisiae

Identifiers

PMID29462149
PMCPMC5834206
OpenAlexW2951422800

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.