Evidence map›Paper›PMID 33856648›Full record

ArticleMolecular neurobiology2021

Semaphorin3F Drives Dendritic Spine Pruning Through Rho-GTPase Signaling.

Bryce W Duncan, Vishwa Mohan, Sarah D Wade, Young Truong, Alexander Kampov-Polevoi, Brenda R Temple, Patricia F Maness

Open access · greenAbstract read
In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 34 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

7 authors at 1 institution in 1 country.

Bryce W Duncan *Department of Biochemistry and Biophysics and Neuroscience Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA.
Vishwa Mohan *Department of Biochemistry and Biophysics and Neuroscience Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA.
Sarah D WadeDepartment of Biochemistry and Biophysics and Neuroscience Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA.
Young TruongDepartment of Biostatistics, School of Global Public Health, University of North Carolina, Chapel Hill, NC, 27599, USA.
Alexander Kampov-PolevoiDepartment of Biochemistry and Biophysics and Neuroscience Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA.
Brenda R TempleDepartment of Biochemistry and Biophysics and Neuroscience Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA.
Patricia F ManessDepartment of Biochemistry and Biophysics and Neuroscience Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA. srclab@med.unc.edu.ORCID http://orcid.org/0000-0003-2481-5610
University of North Carolina at Chapel Hill · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI David Darr · 1985 to 2026
$201.5M
Preclinical CoreP50HD103573 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GABRIEL S DICHTER · 2020 to 2026
$9.7M
Mechanisms of Developmental Spine Pruning Regulated by IgCAMs and SemaphorinsR01MH113280 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MANESS, PATRICIA F · 2017 to 2021
$1.9M
CIT NIH HHS P50HD103573NCI NIH HHS P30 CA016086NICHD NIH HHS P50 HD103573NIMH NIH HHS MH113280NIMH NIH HHS R01 MH113280
6 · The paper itself

Abstract

Dendritic spines of cortical pyramidal neurons are initially overproduced then remodeled substantially in the adolescent brain to achieve appropriate excitatory balance in mature circuits. Here we investigated the molecular mechanism of developmental spine pruning by Semaphorin 3F (Sema3F) and its holoreceptor complex, which consists of immunoglobulin-class adhesion molecule NrCAM, Neuropilin-2 (Npn2), and PlexinA3 (PlexA3) signaling subunits. Structure-function studies of the NrCAM-Npn2 interface showed that NrCAM stabilizes binding between Npn2 and PlexA3 necessary for Sema3F-induced spine pruning. Using a mouse neuronal culture system, we identified a dual signaling pathway for Sema3F-induced pruning, which involves activation of Tiam1-Rac1-PAK1-3 -LIMK1/2-Cofilin1 and RhoA-ROCK1/2-Myosin II in dendritic spines. Inhibitors of actin remodeling impaired spine collapse in the cortical neurons. Elucidation of these pathways expands our understanding of critical events that sculpt neuronal networks and may provide insight into how interruptions to these pathways could lead to spine dysgenesis in diseases such as autism, bipolar disorder, and schizophrenia.

Indexed as

AnimalsCells, CulturedDendritic SpinesHEK293 CellsHumansMembrane ProteinsMiceMice, Inbred C57BLNerve Tissue ProteinsNeuronsrho GTP-Binding ProteinsSignal TransductionMembrane ProteinsNerve Tissue Proteinsrho GTP-Binding ProteinsSEMA3F protein, humanActin cytoskeletonCell adhesion moleculesCortical neuronsDendritic spinesSemaphorinsSignal transductionSpine pruning

Identifiers

PMID33856648
PMCPMC8555654
OpenAlexW3154619346

What OpenQuestion holds

Textmetadata
LicenceTDM
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.