Evidence map›Paper›PMID 38352575›Full record

ArticlebioRxiv : the preprint server for biology2024

Mapping Stress-Responsive Signaling Pathways Induced by Mitochondrial Proteostasis Perturbations.

Nicole Madrazo, Zinia Khattar, Evan T Powers, Jessica D Rosarda, R Luke Wiseman

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Nicole MadrazoDepartment of Molecular and Cellular Biology, Scripps Research, La Jolla, CA 92037.ORCID 0000-0003-3731-0451
Zinia KhattarDepartment of Molecular and Cellular Biology, Scripps Research, La Jolla, CA 92037.
Evan T PowersDepartment of Chemistry, Scripps Research, La Jolla, CA 92037.ORCID 0000-0001-8185-8487
Jessica D RosardaDepartment of Anatomy, Physiology, and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.ORCID 0000-0002-2742-7413
R Luke WisemanDepartment of Molecular and Cellular Biology, Scripps Research, La Jolla, CA 92037.ORCID 0000-0001-9287-6840
Scripps Institution of Oceanography · USUniformed Services University of the Health Sciences · US

Funding

IMPACTING MITOCHONDRIAL FUNCTION THROUGH ALTERED PROTEASE ACTIVITYR01NS095892 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI WISEMAN, ROCKLAND LUKE · 2016 to 2025
$5.3M
Defining Endoplasmic Reticulum Stress-Development Mitochondria RemodelingRF1NS125674 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI WISEMAN, ROCKLAND LUKE · 2022 to 2022
$2.4M
NINDS NIH HHS R01 NS095892NINDS NIH HHS RF1 NS125674
6 · The paper itself

Abstract

Imbalances in mitochondrial proteostasis are associated with pathologic mitochondrial dysfunction implicated in etiologically-diverse diseases. This has led to considerable interest in defining the biological mechanisms responsible for regulating mitochondria in response to mitochondrial stress. Numerous stress responsive signaling pathways have been suggested to regulate mitochondria in response to proteotoxic stress, including the integrated stress response (ISR), the heat shock response (HSR), and the oxidative stress response (OSR). Here, we define the specific stress signaling pathways activated in response to mitochondrial proteostasis stress by monitoring the expression of sets of genes regulated downstream of each of these signaling pathways in published Perturb-seq datasets from K562 cells CRISPRi-depleted of individual mitochondrial proteostasis factors. Interestingly, we find that the ISR is preferentially activated in response to mitochondrial proteostasis stress, with no other pathway showing significant activation. Further expanding this study, we show that broad depletion of mitochondria-localized proteins similarly shows preferential activation of the ISR relative to other stress-responsive signaling pathways. These results both establish our gene set profiling approach as a viable strategy to probe stress responsive signaling pathways induced by perturbations to specific organelles and identify the ISR as the predominant stress-responsive signaling pathway activated in response to mitochondrial proteostasis disruption.

Identifiers

PMID38352575
PMCPMC10862789
OpenAlexW4391672916

What Socratic 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 Socratic graph.