Evidence map›Paper›PMID 35915093›Full record

ArticleNature communications2022

Highly conserved shifts in ubiquitin-proteasome system (UPS) activity drive mitochondrial remodeling during quiescence.

Sibiao Yue, Lei Wang, George N DeMartino, FangZhou Zhao, Yi Liu, Matthew H Sieber

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Finishing the egg.Genetics · 2024
    Article
  8. Article
  9. The role of metabolism in cellular quiescence.Journal of cell science · 2023
    Review
  10. Review
  11. Role of amino acid metabolism in mitochondrial homeostasis.Frontiers in cell and developmental biology · 2023
    Review
  12. 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 1 country.

Sibiao YueDepartment of Physiology, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, 75390, TX, USA.
Lei WangDepartment of Physiology, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, 75390, TX, USA.
George N DeMartinoDepartment of Physiology, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, 75390, TX, USA.
FangZhou ZhaoDepartment of Physiology, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, 75390, TX, USA.
Yi LiuDepartment of Physiology, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, 75390, TX, USA.ORCID 0000-0002-8801-9317
Matthew H SieberDepartment of Physiology, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, 75390, TX, USA. matthew.sieber@utsouthwestern.edu.ORCID 0000-0002-6952-8749
Southwestern Medical CenterSouthwestern Medical Center · US

Funding

UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Jeff G McDonald · 2022 to 2026
$7.4M
Mechanisms of Circadian Clock and Gene Sliencing in NeurosporaR35GM118118 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI LIU, YI · 2016 to 2025
$6.3M
Investigating the role of maternal metabolic reprogramming in progeny physiology and agingR01AG067604 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI SIEBER, MATTHEW · 2020 to 2024
$2.2M
PI31: a regulator of proteasome adaptation to stressR01GM129088 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI DEMARTINO, GEORGE N. · 2019 to 2022
$1.3M
NIA NIH HHS R01 AG067604NIDDK NIH HHS P30 DK127984NIGMS NIH HHS R01 GM129088NIGMS NIH HHS R35 GM118118
6 · The paper itself

Abstract

Defects in cellular proteostasis and mitochondrial function drive many aspects of infertility, cancer, and other age-related diseases. All of these conditions rely on quiescent cells, such as oocytes and adult stem cells, that reduce their activity and remain dormant as part of their roles in tissue homeostasis, reproduction, and even cancer recurrence. Using a multi-organism approach, we show that dynamic shifts in the ubiquitin proteasome system drive mitochondrial remodeling during cellular quiescence. In contrast to the commonly held view that the ubiquitin-proteasome system (UPS) is primarily regulated by substrate ubiquitination, we find that increasing proteasome number and their recruitment to mitochondria support mitochondrial respiratory quiescence (MRQ). GSK3 triggers proteasome recruitment to the mitochondria by phosphorylating outer membrane proteins, such as VDAC, and suppressing mitochondrial fatty acid oxidation. This work defines a process that couples dynamic regulation of UPS activity to coordinated shifts in mitochondrial metabolism in fungi, Drosophila, and mammals during quiescence.

Indexed as

Proteasome Endopeptidase ComplexUbiquitinAnimalsGlycogen Synthase Kinase 3MammalsMitochondriaUbiquitinationGlycogen Synthase Kinase 3Proteasome Endopeptidase ComplexUbiquitin

Identifiers

PMID35915093
PMCPMC9343427
OpenAlexW4289262199

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.