English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/130180
logo share SHARE   Add this article to your Mendeley library MendeleyBASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

The role of thioredoxin-1 (TRX-1) in Caenorhabditis elegans aging

AuthorsGonzález-Barrios, María ; Fierro-González, Juan Carlos; Muñoz, Manuel J. ; Swoboda, Peter; Miranda-Vizuete, Antonio
Issue Date2013
Citation4th Spanish Worm Meeting (2013)
AbstractThioredoxins comprise a conserved family of proteins that mostly depend on their oxidoreductase attributes to reduce disulfide bonds in many target proteins. These redox regulators are involved in many biological processes, including stress resistance and aging. In C. elegans, thioredoxin-1 (TRX-1) is expressed specifically in the ASJ sensory neurons, which have been demonstrated to regulate both dauer formation and longevity. Indeed, we have previously reported that trx-1 (ok1449) null mutants show a decrease in their lifespan while worms overexpressing TRX-1 have a slight increase in lifespan. The reproductive system of C. elegans, among other animals, plays an important role in the regulation of lifespan. For instance, germline deficient mutants glp-1 (e2141) are long lived. In this mutant background, the FOXO transcription factor DAF-16 enters into intestinal nuclei and promotes longevity. This life span extension also requires the activity of the steroid hormone nuclear receptor DAF-12. Insulin signaling is one of the major pathways regulating longevity in all organisms. Mutations in the insulin receptor DAF-2 decrease signaling by this route, leading to the entry of DAF-16 in cell nuclei, where it activates a subset of genes that promote longevity, stress resistance and pathogen avoidance, among others. The mechanisms by which DAF-16 enters intestinal nuclei in daf-2 and glp-1 mutant backgrounds differ. Thus, kri-1, daf-9 and daf-12 are necessary for DAF-16 entry into nuclei in glp-1 mutant background, while they are not necessary for the entry in a daf-2 mutant background. trx-1 (ok1449) significantly suppresses glp-1(e2141) longevity and also suppresses nuclear localization of DAF-16 in intestinal cells but not indaf-2(m577) mutant background, indicating an essential role of trx-1 in the regulation of germ line mediated longevity. Interestingly, trx-1 (ok1449) also suppresses daf-2(e1370) and daf-2(m577) longevity. This dual function in the insulin and germ line pathways has been reported for daf-16 and also for the nuclear hormone receptor daf-12. The fact that trx-1 (ok1449) significantly decreases dauer formation in pdk-1(sa680) mutants when fed with a cholesterol-free diet, while it does not modify dauer formation in a cholesterolsupplemented diet suggests a role of trx-1 in the regulation a nuclear hormone receptor. Indeed, trx-1 (ok1449) downregulates the levels of the DAF-12 direct transcriptional target DAF-9::GFP, in a daf-2 (m577) background. Together, our data support a model where TRX-1 is regulating longevity of the insulin and germ line pathway by modulating, perhaps indirectly, DAF-12 activity.
DescriptionTrabajo presentado al 4th Spanish Worm Meeting, celebrado en Carmona (Sevilla) del 14 al 15 de marzo de 2013.
Appears in Collections:(CABD) Comunicaciones congresos
(IBIS) Comunicaciones congresos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
Show full item record
Review this work

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.