Evidence map›Paper›PMID 27194708›Full record

ArticleThe Plant cell2016

The Proteasome Stress Regulon Is Controlled by a Pair of NAC Transcription Factors in Arabidopsis.

Nicholas P Gladman, Richard S Marshall, Kwang-Hee Lee, Richard D Vierstra

Open access · greenAbstract read
In one paragraph

Article in The Plant cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
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  18. Endoplasmic reticulum-bound ANAC013 factor is cleaved by RHOMBOID-LIKE 2 during the initial response to hypoxia inProceedings of the National Academy of Sciences of the United States of America · 2023
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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

4 authors at 1 institution in 1 country.

Nicholas P GladmanDepartment of Genetics, University of Wisconsin, Madison, Wisconsin 53706.
Richard S MarshallDepartment of Genetics, University of Wisconsin, Madison, Wisconsin 53706 Department of Biology, Washington University in St. Louis, St. Louis, Missouri 63130.
Kwang-Hee LeeDepartment of Genetics, University of Wisconsin, Madison, Wisconsin 53706.
Richard D VierstraDepartment of Genetics, University of Wisconsin, Madison, Wisconsin 53706 Department of Biology, Washington University in St. Louis, St. Louis, Missouri 63130 rdvierstra@wustl.edu.ORCID 0000-0003-0210-3516
University of Wisconsin–Madison · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007133 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI PERNA, NICOLE T · 1985 to 2023
$16.5M
NIGMS NIH HHS T32 GM007133
6 · The paper itself

Abstract

Proteotoxic stress, which is generated by the accumulation of unfolded or aberrant proteins due to environmental or cellular perturbations, can be mitigated by several mechanisms, including activation of the unfolded protein response and coordinated increases in protein chaperones and activities that direct proteolysis, such as the 26S proteasome. Using RNA-seq analyses combined with chemical inhibitors or mutants that induce proteotoxic stress by impairing 26S proteasome capacity, we defined the transcriptional network that responds to this stress in Arabidopsis thaliana This network includes genes encoding core and assembly factors needed to build the complete 26S particle, alternative proteasome capping factors, enzymes involved in protein ubiquitylation/deubiquitylation and cellular detoxification, protein chaperones, autophagy components, and various transcriptional regulators. Many loci in this proteasome-stress regulon contain a consensus cis-element upstream of the transcription start site, which was previously identified as a binding site for the NAM/ATAF1/CUC2 78 (NAC78) transcription factor. Double mutants disrupting NAC78 and its closest relative NAC53 are compromised in the activation of this regulon and notably are strongly hypersensitive to the proteasome inhibitors MG132 and bortezomib. Given that NAC53 and NAC78 homo- and heterodimerize, we propose that they work as a pair in activating the expression of numerous factors that help plants survive proteotoxic stress and thus play a central regulatory role in maintaining protein homeostasis.

Indexed as

ArabidopsisArabidopsis ProteinsBortezomibGene Expression Regulation, PlantLeupeptinsProteasome Endopeptidase ComplexProtein BindingRegulonTranscription FactorsArabidopsis ProteinsATP dependent 26S proteasebenzyloxycarbonylleucyl-leucyl-leucine aldehydeBortezomibLeupeptinsProteasome Endopeptidase ComplexTranscription Factors

Identifiers

PMID27194708
PMCPMC4944403
OpenAlexW2400582439

What OpenQuestion holds

Textmetadata
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.