Evidence map›Paper›PMID 37662186›Full record

ArticlebioRxiv : the preprint server for biology2023

Cytoskeletal adaptation following long-term dysregulation of actomyosin in neuronal processes.

Bruno A Cisterna, Kristen Skruber, Makenzie L Jane, Caleb I Camesi, Ivan D Nguyen, Peyton V Warp, Joseph B Black, Mitchell T Butler, James E Bear, Read Tracy-Ann and 1 more

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. 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

11 authors at 5 institutions in 1 country.

Bruno A CisternaDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, USA.
Kristen SkruberDepartment of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, CA, USA.
Makenzie L JaneDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, USA.
Caleb I CamesiDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, USA.
Ivan D NguyenDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, USA.
Peyton V WarpUniversity of Miami Miller School of Medicine, Miami, FL, USA.
Joseph B BlackDivision of Urologic Surgery, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Mitchell T ButlerDepartment of Cell Biology and Physiology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
James E BearDepartment of Cell Biology and Physiology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Read Tracy-AnnDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, USA.
Eric A VitriolDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, USA.
Augusta University · USUniversity of North Carolina at Chapel Hill · USBeth Israel Deaconess Medical Center · USUniversity of California, San Francisco · USUniversity of Miami · US

Funding

Deciphering the Mechanisms and Cellular Roles of Monomer-Driven Actin DynamicsR35GM137959 · NIGMS · UNIVERSITY OF FLORIDA · PI VITRIOL, ERIC A · 2020 to 2024
$2.3M
NIGMS NIH HHS R35 GM137959
6 · The paper itself

Abstract

Microtubules, intermediate filaments, and actin are cytoskeletal polymer networks found within the cell. While each has unique functions, all the cytoskeletal elements must work together for cellular mechanics to be fully operative. This is achieved through crosstalk mechanisms whereby the different networks influence each other through signaling pathways and direct interactions. Because crosstalk can be complex, it is possible for perturbations in one cytoskeletal element to affect the others in ways that are difficult to predict. Here we investigated how long-term changes to the actin cytoskeleton affect microtubules and intermediate filaments. Reducing F-actin or actomyosin contractility increased acetylated microtubules and intermediate filament expression, with the effect being significantly more pronounced in neuronal processes. Changes to microtubules were completely reversible if F-actin and myosin activity is restored. Moreover, the altered microtubules in neuronal processes resulting from F-actin depletion caused significant changes to microtubule-based transport, mimicking phenotypes that are linked to neurodegenerative disease. Thus, defects in actin dynamics cause a compensatory response in other cytoskeleton components which profoundly alters cellular function.

Identifiers

PMID37662186
PMCPMC10473725
OpenAlexW4386203799

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.