Evidence map›Paper›PMID 27078101›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Novel DLK-independent neuronal regeneration in Caenorhabditis elegans shares links with activity-dependent ectopic outgrowth.

Samuel H Chung, Mehraj R Awal, James Shay, Melissa M McLoed, Eric Mazur, Christopher V Gabel

Abstract readComment
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Article
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  6. Dendrite glia interactions: lessons from theFrontiers in cell and developmental biology · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Samuel H ChungSchool of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138; Department of Physiology and Biophysics, Boston University School of Medicine, Boston, MA 02118; Boston University Photonics Center, Boston, MA 02215;ORCID 0000-0003-2553-1396
Mehraj R AwalDepartment of Physiology and Biophysics, Boston University School of Medicine, Boston, MA 02118; Boston University Photonics Center, Boston, MA 02215;
James ShayDepartment of Physiology and Biophysics, Boston University School of Medicine, Boston, MA 02118; Boston University Photonics Center, Boston, MA 02215;
Melissa M McLoedDepartment of Physiology and Biophysics, Boston University School of Medicine, Boston, MA 02118; Boston University Photonics Center, Boston, MA 02215;
Eric MazurSchool of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138; Department of Physics, Harvard University, Cambridge, MA 02138.
Christopher V GabelDepartment of Physiology and Biophysics, Boston University School of Medicine, Boston, MA 02118; Boston University Photonics Center, Boston, MA 02215; cvgabel@bu.edu.

Funding

TRAINING IN BIOMOLECULAR PHARMACOLOGYT32GM008541 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FARB, DAVID H · 1997 to 2022
$5.2M
C. elegans model for mammalian lesion-conditioned axon regenerationR21NS078580 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GABEL, CHRISTOPHER V · 2012 to 2013
$419k
NIGMS NIH HHS T32 GM008541NINDS NIH HHS R21 NS078580
6 · The paper itself

Abstract

During development, a neuron transitions from a state of rapid growth to a stable morphology, and neurons within the adult mammalian CNS lose their ability to effectively regenerate in response to injury. Here, we identify a novel form of neuronal regeneration, which is remarkably independent of DLK-1/DLK, KGB-1/JNK, and other MAPK signaling factors known to mediate regeneration in Caenorhabditis elegans, Drosophila, and mammals. This DLK-independent regeneration in C. elegans has direct genetic and molecular links to a well-studied form of endogenous activity-dependent ectopic axon outgrowth in the same neuron type. Both neuron outgrowth types are triggered by physical lesion of the sensory dendrite or mutations disrupting sensory activity, calcium signaling, or genes that restrict outgrowth during neuronal maturation, such as SAX-1/NDR kinase or UNC-43/CaMKII. These connections suggest that ectopic outgrowth represents a powerful platform for gene discovery in neuronal regeneration. Moreover, we note numerous similarities between C. elegans DLK-independent regeneration and lesion conditioning, a phenomenon producing robust regeneration in the mammalian CNS. Both regeneration types are triggered by lesion of a sensory neurite via reduction of neuronal activity and enhanced by disrupting L-type calcium channels or elevating cAMP. Taken as a whole, our study unites disparate forms of neuronal outgrowth to uncover fresh molecular insights into activity-dependent control of the adult nervous system's intrinsic regenerative capacity.

Indexed as

Nerve RegenerationAnimalsAxonsCaenorhabditis elegansCaenorhabditis elegans ProteinsCalcium Channels, L-TypeCaenorhabditis elegans ProteinsCalcium Channels, L-Typeactivity-dependent ectopic axon outgrowthaxon regenerationDLK-1femtosecond laser ablationlesion conditioning

Identifiers

PMID27078101
PMCPMC4878464

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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.