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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)

Project description

The role of stress on cellular ageing

Cellular ageing is an enigmatic process with many of its aspects remaining poorly understood. The key objective of the EU-funded NARESICA project is to investigate the role of stress on the ageing process. Using telomere length as a biomarker of ageing, researchers will study how chronic stress and in particular glucocorticoid stress hormones accelerate ageing in two avian species. Emphasis will be placed on a number of potential drivers of ageing such as mitochondrial function, oxidative stress, DNA damage and mTOR cellular signalling. Collectively, the project's findings will unveil important information on a fundamental biological process with clinical implications.

Objective

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.

Coordinator

UNIVERSITE LYON 1 CLAUDE BERNARD
Net EU contribution
€ 184 707,84
Address
BOULEVARD DU 11 NOVEMBRE 1918 NUM43
69622 Villeurbanne Cedex
France

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Region
Auvergne-Rhône-Alpes Rhône-Alpes Rhône
Activity type
Higher or Secondary Education Establishments
Links
Total cost
€ 184 707,84