Department of Neurobiology; Alkema Lab; Byrne Lab; Graduate School of Biomedical Sciences
Genetics and Genomics | Nervous System | Neuroscience and Neurobiology
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.
Axons, Diapause, Neurons, Neuronal morphology, Touch, Caenorhabditis elegans, Larvae
Rights and Permissions
Copyright: © 2019 Caneo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
DOI of Published Version
PLoS Genet. 2019 Jan 14;15(1):e1007863. doi: 10.1371/journal.pgen.1007863. eCollection 2019 Jan. Link to article on publisher's site
Caneo M, Julian V, Byrne AB, Alkema MJ, Calixto A. (2019). Diapause induces functional axonal regeneration after necrotic insult in C. elegans. Open Access Publications by UMass Chan Authors. https://doi.org/10.1371/journal.pgen.1007863. Retrieved from https://escholarship.umassmed.edu/oapubs/3715
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.