Evidence map›Paper›PMID 31042147›Full record

ArticleeLife2019

Structural plasticity of actin-spectrin membrane skeleton and functional role of actin and spectrin in axon degeneration.

Guiping Wang, David J Simon, Zhuhao Wu, Deanna M Belsky, Evan Heller, Melanie K O'Rourke, Nicholas T Hertz, Henrik Molina, Guisheng Zhong, Marc Tessier-Lavigne and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 72 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

11 authors at 3 institutions in 1 country.

Guiping Wang *Department of Chemistry and Chemical Biology, Howard Hughes Medical Institute, Harvard University, Cambridge, United States.
David J Simon *Laboratory of Brain Development and Repair, The Rockefeller University, New York, United States.ORCID 0000-0002-2683-5757
Zhuhao WuLaboratory of Brain Development and Repair, The Rockefeller University, New York, United States.ORCID 0000-0002-2471-0555
Deanna M BelskyDepartment of Biology, Stanford University, Stanford, United States.
Evan HellerDepartment of Chemistry and Chemical Biology, Howard Hughes Medical Institute, Harvard University, Cambridge, United States.
Melanie K O'RourkeDepartment of Biology, Stanford University, Stanford, United States.
Nicholas T HertzLaboratory of Brain Development and Repair, The Rockefeller University, New York, United States.
Henrik MolinaProteomics Resource Center, The Rockefeller University, New York, United States.
Guisheng ZhongDepartment of Chemistry and Chemical Biology, Howard Hughes Medical Institute, Harvard University, Cambridge, United States.
Marc Tessier-LavigneLaboratory of Brain Development and Repair, The Rockefeller University, New York, United States.
Xiaowei ZhuangDepartment of Chemistry and Chemical Biology, Howard Hughes Medical Institute, Harvard University, Cambridge, United States.ORCID 0000-0002-6034-7853
Rockefeller University · USHoward Hughes Medical Institute · USStanford University · US

Funding

Generation of novel cell type specific mouse genetic toolsU19MH114830 · NIMH · ALLEN INSTITUTE · PI NGAI, JOHN J. · 2017 to 2021
$64.7M
Regulation of axon degeneration by the apoptotic pathwayR01NS089786 · NINDS · STANFORD UNIVERSITY · PI TESSIER-LAVIGNE, MARC · 2014 to 2018
$2.8M
Illuminating molecular mechanisms of cellular functions by single-molecule and super-resolution imagingR35GM122487 · NIGMS · HARVARD UNIVERSITY · PI ZHUANG, XIAOWEI · 2017 to 2021
$2.1M
NIGMS NIH HHS R35 GM122487NIH HHS R01NS089786NIH HHS R35GM122487NIMH NIH HHS U19 MH114830NINDS NIH HHS R01 NS089786
6 · The paper itself

Abstract

Axon degeneration sculpts neuronal connectivity patterns during development and is an early hallmark of several adult-onset neurodegenerative disorders. Substantial progress has been made in identifying effector mechanisms driving axon fragmentation, but less is known about the upstream signaling pathways that initiate this process. Here, we investigate the behavior of the actin-spectrin-based Membrane-associated Periodic Skeleton (MPS), and effects of actin and spectrin manipulations in sensory axon degeneration. We show that trophic deprivation (TD) of mouse sensory neurons causes a rapid disassembly of the axonal MPS, which occurs prior to protein loss and independently of caspase activation. Actin destabilization initiates TD-related retrograde signaling needed for degeneration; actin stabilization prevents MPS disassembly and retrograde signaling during TD. Depletion of βII-spectrin, a key component of the MPS, suppresses retrograde signaling and protects axons against degeneration. These data demonstrate structural plasticity of the MPS and suggest its potential role in early steps of axon degeneration.

Indexed as

Nerve DegenerationActinsAnimalsCell MembraneCells, CulturedCytoskeletonMiceSensory Receptor CellsSignal TransductionSpectrinActinsSpectrinactinaxon degenerationcell biologycytoskeletonmouseneuroscienceneurotrophinsspectrinsuper-resolution microscopy

Identifiers

PMID31042147
PMCPMC6494423
OpenAlexW2943131619

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.