Evidence map›Paper›PMID 32349127›Full record

ArticleThe Journal of cell biology2020

Stress sensor Ire1 deploys a divergent transcriptional program in response to lipid bilayer stress.

Nurulain Ho, Wei Sheng Yap, Jiaming Xu, Haoxi Wu, Jhee Hong Koh, Wilson Wen Bin Goh, Bhawana George, Shu Chen Chong, Stefan Taubert, Guillaume Thibault

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.4field-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

51 citing papers in PubMed, 78 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Nurulain HoLipid Regulation and Cell Stress Group, School of Biological Sciences, Nanyang Technological University, Singapore.
Wei Sheng YapLipid Regulation and Cell Stress Group, School of Biological Sciences, Nanyang Technological University, Singapore.
Jiaming XuCentre for Molecular Medicine and Therapeutics, British Columbia Children's Hospital Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
Haoxi WuLipid Regulation and Cell Stress Group, School of Biological Sciences, Nanyang Technological University, Singapore.
Jhee Hong KohLipid Regulation and Cell Stress Group, School of Biological Sciences, Nanyang Technological University, Singapore.
Wilson Wen Bin GohBio-Data Science and Education Research Group, School of Biological Sciences, Nanyang Technological University, Singapore.
Bhawana GeorgeLipid Regulation and Cell Stress Group, School of Biological Sciences, Nanyang Technological University, Singapore.
Shu Chen ChongLipid Regulation and Cell Stress Group, School of Biological Sciences, Nanyang Technological University, Singapore.
Stefan TaubertCentre for Molecular Medicine and Therapeutics, British Columbia Children's Hospital Research Institute, Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
Guillaume ThibaultLipid Regulation and Cell Stress Group, School of Biological Sciences, Nanyang Technological University, Singapore.
Nanyang Technological University · SGUniversity of British Columbia · CAAgency for Science, Technology and Research · SG

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
CIHR PJT-153199NIH HHS P40 OD010440
6 · The paper itself

Abstract

Membrane integrity at the endoplasmic reticulum (ER) is tightly regulated, and its disturbance is implicated in metabolic diseases. Using an engineered sensor that activates the unfolded protein response (UPR) exclusively when normal ER membrane lipid composition is compromised, we identified pathways beyond lipid metabolism that are necessary to maintain ER integrity in yeast and in C. elegans. To systematically validate yeast mutants that disrupt ER membrane homeostasis, we identified a lipid bilayer stress (LBS) sensor in the UPR transducer protein Ire1, located at the interface of the amphipathic and transmembrane helices. Furthermore, transcriptome and chromatin immunoprecipitation analyses pinpoint the UPR as a broad-spectrum compensatory response wherein LBS and proteotoxic stress deploy divergent transcriptional UPR programs. Together, these findings reveal the UPR program as the sum of two independent stress responses, an insight that could be exploited for future therapeutic intervention.

Indexed as

Unfolded Protein ResponseAnimalsBiosensing TechniquesCaenorhabditis elegansCaenorhabditis elegans ProteinsChromatinEndoplasmic ReticulumEndoplasmic Reticulum StressGene Expression ProfilingGene Expression RegulationGenes, ReporterGreen Fluorescent ProteinsHeat-Shock ProteinsHomeostasisIntracellular MembranesLipid BilayersCaenorhabditis elegans ProteinsChromatinGreen Fluorescent ProteinsHeat-Shock ProteinsHsp-4 protein, C elegansIRE1 protein, S cerevisiaeLipid BilayersLuminescent ProteinsMembrane GlycoproteinsProtein Serine-Threonine KinasesRed Fluorescent ProteinSaccharomyces cerevisiae Proteins

Identifiers

PMID32349127
PMCPMC7337508
OpenAlexW3018410811

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.