Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters











Database
Language
Publication year range
1.
PLoS Genet ; 15(1): e1007863, 2019 01.
Article in English | MEDLINE | ID: mdl-30640919

ABSTRACT

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.


Subject(s)
Axons , Caenorhabditis elegans Proteins/genetics , MAP Kinase Kinase Kinases/genetics , Membrane Proteins/genetics , Nerve Regeneration/genetics , Nervous System Malformations/genetics , Animals , Caenorhabditis elegans/genetics , Caenorhabditis elegans/growth & development , Diapause/genetics , Diapause/physiology , Gene Expression Regulation, Developmental , Necrosis/genetics , Necrosis/pathology , Nervous System Malformations/physiopathology , Nervous System Malformations/rehabilitation , Sensory Receptor Cells/metabolism , Touch/genetics
SELECTION OF CITATIONS
SEARCH DETAIL