Vista simple de metadatos

dc.contributor.authorCaneo, Mauricio; Calixto, Andrea [Univ Mayor, Fac Ciencias, Ctr Genom & Bioinformat, Santiago, Chile]es_CL
dc.contributor.authorJulian, Víctoriaes_CL
dc.contributor.authorByrne, Alexandra B.es_CL
dc.contributor.authorAlkema, Mark J.es_CL
dc.contributor.authorCalixto, Andreaes_CL
dc.date.accessioned2020-04-12T14:11:55Z
dc.date.accessioned2020-04-14T15:46:19Z
dc.date.available2020-04-12T14:11:55Z
dc.date.available2020-04-14T15:46:19Z
dc.date.issued2019es_CL
dc.identifier.citationCaneo, M., Julian, V., Byrne, A. B., Alkema, M. J., & Calixto, A. (2019). Diapause induces functional axonal regeneration after necrotic insult in C. elegans. PLoS genetics, 15(1), e1007863.es_CL
dc.identifier.issn1553-7404es_CL
dc.identifier.urihttps://doi.org/10.1371/journal.pgen.1007863es_CL
dc.identifier.urihttp://repositorio.umayor.cl/xmlui/handle/sibum/6731
dc.description.abstractMany 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. Author summary Diapause entry and hibernation have the striking ability to protect the nervous system from diverse types of damage. Here we show that the diapausing dauer larvae of C. elegans regenerate broken mechanosensory neurons that were damaged by the hyperactivation of degenerins (MEC-4d) or by axotomy during diapause. This regeneration is complete and functional, rendering neurons capable of responding to touch after three days in diapause. Genetic inactivation of the insulin receptor DAF-2 promotes regeneration of mec-4d axons in non-dauer animals. Overexpression of the downstream transcription factor DAF-16 promotes neuronal protection in mec-4d neurons while loss of daf-16 accelerates mec-4d induced degeneration. Temperature sensitive activation of DAF-2 during diapause induces the loss of axonal integrity. This indicates that the insulin signaling pathway is an important underlying factor in regeneration. Additionally, we show that complete morphological regeneration depends on DLK-1, a conserved protein required for axonal repair. In this work we introduce a simple model of complete axonal regeneration, which will greatly facilitate the study of environmental and genetic factors affecting neurodegeneration and constitute an advantage in studying axonal regrowth.es_CL
dc.description.sponsorshipFondo Nacional de Ciencia y Tecnologia, Chile [1131038]; Comision Nacional de Investigacion Cientifica y Tecnologica [2013-0041]; Millennium InstituteTakeda Pharmaceutical Company Ltd; Millennium Scientific Initiative of the Chilean Ministry of Economy, Development, and Tourism [P029-022-F]; National Institute of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [GM084491]es_CL
dc.description.sponsorshipThe study was supported by the Fondo Nacional de Ciencia y Tecnologia, Chile (grant number 1131038) to AC, the Comision Nacional de Investigacion Cientifica y Tecnologica (grant 2013-0041) to AC, The Millennium Institute supported by the Millennium Scientific Initiative of the Chilean Ministry of Economy, Development, and Tourism (P029-022-F) to AC and the National Institute of Health (grant GM084491) to MJA. The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.es_CL
dc.language.isoenes_CL
dc.publisherPUBLIC LIBRARY SCIENCEes_CL
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourcePLoS Genet., ENE, 2019. 15(1)
dc.subjectGenetics & Heredityes_CL
dc.titleDiapause induces functional axonal regeneration after necrotic insult in C. eleganses_CL
dc.typeArtículoes_CL
umayor.facultadCIENCIAS
umayor.politicas.sherpa/romeoDOAJ Gold, Green Publishedes_CL
umayor.indexadoWOS:000457395500016es_CL
umayor.indexadoPMID: 30640919es_CL
dc.identifier.doiDOI: 10.1371/journal.pgen.1007863es_CL]
umayor.indicadores.wos-(cuartil)Q1es_CL
umayor.indicadores.scopus-(scimago-sjr)SCIMAGO/ INDICE H: 194 Hes_CL


Vista simple de metadatos



Modificado por: Sistema de Bibliotecas Universidad Mayor - SIBUM
DSpace software copyright © 2002-2018  DuraSpace