MITODR
Determination of evolutionary conserved genes that respond to reduced food intake through mitochondria signaling to affect aging
| Coordinatore |
Organization address
address: Rue Michel -Ange 3 contact info |
| Nazionalità Coordinatore | Non specificata |
| Totale costo | 50˙000 € |
| EC contributo | 50˙000 € |
| Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | FP7-PEOPLE-2009 |
| Anno di inizio | 2011 |
| Periodo (anno-mese-giorno) | 2011-01-01 - 2012-12-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE
Organization address
address: Rue Michel -Ange 3 contact info |
FR (PARIS) | coordinator | 50˙000.00 |
Mappa
Word cloud
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
Obiettivo del progetto (Objective)
'The links between diet and lifespan have been revealed 70 years ago but still constitute one of the most mysterious, exciting and extensively studied areas in aging research. In various organisms tested, a restriction of food intake, or DR, can result in lifespan extension up to 50%. In rodents and nonhuman primates, the beneficial effect of DR on longevity is accompanied by reduced incidence of age-related diseases. Thus, as world populations age, understanding how DR impacts animal physiology has far-reaching potentials in term of public health. Recent research has shown that the mitochondrion organelle play an important and evolutionary conserved role in mediating physiologic effects of DR. Our project aims to uncover the molecular changes induced by mitochondria upon DR in C. elegans. We propose to identify genes downstream of mitochondria that affect animal physiology and in particular lifespan upon DR. The nematode C. elegans is an excellent model for this project because of its many powerful genetic and genomic tools. In our first objective, we plan to generate a novel DR model in C. elegans based on its mitochondrial component using chemical and genetics mimics. In our second objective, we propose to identify the gene expression changes specifically induced by mitochondria upon DR. This proposal is likely to reveal new mediators of the cellular adaptations induced by reduced food intake. In addition, our findings will also greatly improve the understanding of mitochondrial signal transduction in controlling whole organism physiology and aging processes. In the future, our research may contribute to therapeutic development of mitochondria-targeted strategies to benefit healthy aging and alleviate age-related diseases.'