Evidence map›Paper›PMID 33090183›Full record

ArticleThe Journal of cell biology2020

ER-mitochondria contacts promote mitochondrial-derived compartment biogenesis.

Alyssa M English, Max-Hinderk Schuler, Tianyao Xiao, Benoît Kornmann, Janet M Shaw, Adam L Hughes

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 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  9. Molecular mechanisms of mitochondrial dynamics.Nature reviews. Molecular cell biology · 2025
    Review
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  19. Review
  20. The emerging mechanisms and functions of microautophagy.Nature reviews. Molecular cell biology · 2023
    Review
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

6 authors at 2 institutions in 2 countries.

Alyssa M EnglishDepartment of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT.
Max-Hinderk SchulerDepartment of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT.
Tianyao XiaoDepartment of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT.
Benoît KornmannDepartment of Biochemistry, University of Oxford, Oxford, UK.
Janet M ShawDepartment of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT.
Adam L HughesDepartment of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT.
University of Utah · USUniversity of Oxford · GB

Funding

TRAINING PROGRAM IN GENETICST32GM007464 · NIGMS · UNIVERSITY OF UTAH · PI GRUNWALD, DAVID J., STANFIELD, GILLIAN · 1985 to 2020
$6.1M
REGULATION OF MITOCHONDRIAL INHERITANCE IN YEASTR01GM053466 · NIGMS · UNIVERSITY OF UTAH · PI SHAW, JANET M. · 1996 to 2013
$4.6M
Regulation of Mitochondrial HomeostasisR35GM119694 · NIGMS · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Adam Hughes · 2016 to 2026
$4.2M
The Role of the Lysosome in AgingR01AG061376 · NIA · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Adam Hughes · 2018 to 2026
$3.3M
Mechanisms of Mitochondrial DistributionR01GM084970 · NIGMS · UNIVERSITY OF UTAH · PI SHAW, JANET M. · 2008 to 2017
$2.8M
Role of Mitophagy in Mitochondrial Protein Quality ControlR00AG043095 · NIA · UNIVERSITY OF UTAH · PI HUGHES, ADAM · 2014 to 2016
$740k
The Role of the Lysosome in AgingR56AG055648 · NIA · UNIVERSITY OF UTAH · PI HUGHES, ADAM · 2017 to 2017
$379k
Role of Mitophagy in Mitochondrial Protein Quality ControlK99AG043095 · NIA · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HUGHES, ADAM · 2013 to 2013
$90k
Howard Hughes Medical InstituteNIA NIH HHS K99 AG043095NIA NIH HHS R00 AG043095NIA NIH HHS R01 AG061376NIA NIH HHS R56 AG055648NIGMS NIH HHS R01 GM053466NIGMS NIH HHS R01 GM084970NIGMS NIH HHS R35 GM119694NIGMS NIH HHS T32 GM007464Wellcome TrustWellcome Trust 214291/Z/18/Z
6 · The paper itself

Abstract

Mitochondria are dynamic organelles with essential roles in signaling and metabolism. We recently identified a cellular structure called the mitochondrial-derived compartment (MDC) that is generated from mitochondria in response to amino acid overabundance stress. How cells form MDCs is unclear. Here, we show that MDCs are dynamic structures that form and stably persist at sites of contact between the ER and mitochondria. MDC biogenesis requires the ER-mitochondria encounter structure (ERMES) and the conserved GTPase Gem1, factors previously implicated in lipid exchange and membrane tethering at ER-mitochondria contacts. Interestingly, common genetic suppressors of abnormalities displayed by ERMES mutants exhibit distinct abilities to rescue MDC formation in ERMES-depleted strains and are incapable of rescuing MDC formation in cells lacking Gem1. Thus, the function of ERMES and Gem1 in MDC biogenesis may extend beyond their conventional role in maintaining mitochondrial phospholipid homeostasis. Overall, this study identifies an important function for ER-mitochondria contacts in the biogenesis of MDCs.

Indexed as

Organelle BiogenesisEndoplasmic ReticulumMitochondriaMutationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsGEM1 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID33090183
PMCPMC7588143
OpenAlexW3093562399

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.