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Mechanisms linking stress and ageing in two avian species exhibiting contrasted natural resistance to stress (NAtural REsistance to Stress-Induced Cellular Ageing)

Description du projet

Le rôle du stress dans le vieillissement cellulaire

Le vieillissement cellulaire est un processus énigmatique dont nombre d’aspects restent encore méconnus. L’objectif principal du projet NARESICA, financé par l’UE, consiste à étudier le rôle du stress dans le processus de vieillissement. En utilisant la longueur des télomères comme biomarqueur du vieillissement, les chercheurs étudieront la manière dont le stress chronique et, en particulier, les glucocorticoïdes (hormones du stress) accélèrent le vieillissement chez deux espèces aviaires. L’accent sera placé sur plusieurs moteurs potentiels du vieillissement, tels que la fonction mitochondriale, le stress oxydatif, les lésions de l’ADN et la voie de signalisation cellulaire mTOR. Dans l’ensemble, les conclusions du projet dévoileront des informations importantes sur un processus biologique fondamental ayant des implications cliniques.

Objectif

Previous research has identified stress exposure as a key factor influencing health state and ageing rate. The overall aim of the proposed project is to investigate the precise mechanisms linking stress exposure to accelerated cellular ageing (using telomere length as a biomarker of ageing), and to identify potential mechanisms allowing some species to better prevent stress-induced ageing than others. To this aim I will use two avian species (Japanese quail and king penguin) to investigate (1) if chronic stress affects telomere shortening differently between species exhibiting contrasted stress resistance, (2) if glucocorticoid ‘stress’ hormones are directly responsible of the stress-induced alterations in telomere dynamics, (3) by which mechanisms (i.e. alterations of mitochondrial function, oxidative stress and DNA damage, impaired mTOR cellular signalling or telomere maintenance) stress exposure is accelerating telomere shortening, and if king penguin have specific mechanisms preventing/limiting stress-induced telomere shortening, and (4) if chronic stress / glucocorticoid hormones modify the acute oxidative stress responses of individuals. To this end, I will employ experimental approaches manipulating stress exposure and glucocorticoid hormones in captive Japanese quail and wild king penguins, and measure the resulting impact on telomere shortening and its potential cellular drivers (mitochondrial function, oxidative stress, mTOR cellular signalling). This project will enable a two-way transfer of skills and competences between the applicant and the host, by providing training to the applicant regarding mitochondrial biology, cellular signalling and gene expression, and by providing the host with the opportunity to integrate an ageing component through the use of telomeres in his current and future projects.

Coordinateur

UNIVERSITE LYON 1 CLAUDE BERNARD
Contribution nette de l'UE
€ 184 707,84
Adresse
BOULEVARD DU 11 NOVEMBRE 1918 NUM43
69622 Villeurbanne Cedex
France

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Région
Auvergne-Rhône-Alpes Rhône-Alpes Rhône
Type d’activité
Higher or Secondary Education Establishments
Liens
Coût total
€ 184 707,84