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Diapause induces functional axonal regeneration after necrotic insult in C. elegans
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Diapause induces functional axonal regeneration after necrotic insult in C. elegans
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Diapause induces functional axonal regeneration after necrotic insult in C. elegans
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Journal Article
Diapause induces functional axonal regeneration after necrotic insult in C. elegans
2019
Overview
Many neurons are unable to regenerate after damage. The ability to regenerate after an insult depends on life stage, neuronal subtype, intrinsic and extrinsic factors. C. elegans is a powerful model to test the genetic and environmental factors that affect axonal regeneration after damage, since its axons can regenerate after neuronal insult. Here we demonstrate that diapause promotes the complete morphological regeneration of truncated touch receptor neuron (TRN) axons expressing a neurotoxic MEC-4(d) DEG/ENaC channel. Truncated axons of different lengths were repaired during diapause and we observed potent axonal regrowth from somas alone. Complete morphological regeneration depends on DLK-1 but neuronal sprouting and outgrowth is DLK-1 independent. We show that TRN regeneration is fully functional since animals regain their ability to respond to mechanical stimulation. Thus, diapause induced regeneration provides a simple model of complete axonal regeneration which will greatly facilitate the study of environmental and genetic factors affecting the rate at which neurons die.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Axons
/ Caenorhabditis elegans - genetics
/ Caenorhabditis elegans - growth & development
/ Caenorhabditis elegans Proteins - genetics
/ Diapause
/ Gene Expression Regulation, Developmental
/ Lasers
/ MAP Kinase Kinase Kinases - genetics
/ Medicine and Health Sciences
/ Membrane Proteins - genetics
/ Mutation
/ Nerve Regeneration - genetics
/ Nervous System Malformations - genetics
/ Nervous System Malformations - physiopathology
/ Nervous System Malformations - rehabilitation
/ Neurons
/ Research and Analysis Methods
/ Sensory Receptor Cells - metabolism
/ Worms
