Objectif
The overall aim of this program is to assess the role of mitochondrial function in ageing and life span control. The strategy that we shall use is to discover mechanisms that show evolutionary conservation between invertebrate and mammalian model systems. We will use a unique matrix of model organisms (yeast, Podospora anserina, Caenorhabditis elegans, Drosophila melanogaster, mouse and rat) and cell culture systems. Specific questions will be experimentally tested. The following age-related issues are addr essed: (i) modulation of mitochondrial reactive oxygen species (ROS) by different means, (ii) relevance of molecular and cellular pathways to maintain a "healthy" population of mitochondria, (iii) nature and impact of signalling pathways on mitochondrial a ctivity, (iv) effects of dietary restriction on mitochondrial activity, (v) novel age-related mitochondrial functions. The participating laboratories have a strong commitment for collaborative work and ideally complement each other. Some of the partners ex tensively collaborated in the past or are collaborating presently in the field of research addressed in this IP. They are working with different model organisms and systems, most are well experienced in the field of experimental biogerontology, and they ea ch have a specific expertise in different fields of research ranging from advanced biochemistry, cytology, genetics to molecular biology. This consortium will be in the unique situation to perform competitive research with other programs in the world aimed to identify and characterize mechanisms of ageing that are conserved in most species, hence called 'public' mechanisms of ageing. At the same time, the IP will complement European activities that follow other strategies (e.g. comparing mitochondrial para meters from human tissues of different human populations) to elucidate the role of mitochondria in human ageing.'
Champ scientifique
Mots‑clés
Appel à propositions
FP6-2003-LIFESCIHEALTH-I
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