Our Projects

In modern societies, human mean lifespan has steadily increased over the past 30 years. On the other hand, birth rates are low. Thus, societies get older altogether and we have to face an unprecedented epidemic of age-related diseases such as cancer, metabolic syndromes, neurodegenerative disease and sarcopenia. While much effort is dedicated to the understanding of each one of these diseases, it is also possible to delay the aging process itself. This approach is now recognized to be very promising. Our research aims at identifying critical targets of the aging process that may become key therapeutic target to fight age-related diseases.

• Reproduction and Aging 

The germline was recently shown to affect both longevity and fat storage (Hsin et al, Nature, 1999, Wang et al, Science, 2009). Moreover, similar observations were made in Drosophila, suggesting that this is a conserved mechanism (Flatt et al, PNAS, 2007). Our lab uses genetic and biochemistry to find genes that link aging, reproduction and fat metabolism. Our goal is to bring strong experimental answers to fundamental questions such as What metabolic changes support lifespan extension?

• Genetics of Dietary Restriction

Lowering food intake without malnutrition extends lifespan in many species. We are investigating the genetic basis of the Dietary Restriction response. Our goal is to identify key genes that can mimic DR.

• Aging at the single cell level

We are working with Gilles Charvin's group at the IGBMC in Strasbourg to study aging at the single cell level using S. cerevisiae. We combine micro-fluidic devices with basic genetics to tackle some of the key questions in the field. 

            1. How can we explain the variability in mean lifespan in a isogenic population? 

            2. Out of all age-related events, what comes first?

• Fat metabolism and aging

This has become one of the key question in our lab. The importance of nuclear receptor signaling in the regulation of longevity suggest that fat metabolism may be linked to longevity. But how does this work?

We have shown that fatty acid desaturation is fully required to extend lifespan by ablation of the germ line. Is it sufficient?

All longevity mutants harbor singular metabolic traits. Is there a "metabolic signature" that sustain long life? and if so, how can it be most specifically described?

Our lab is actively working on these rather complex questions by studying different longevity mutants that harbor obvious "fat" phenotypes such as daf-2 or glp-1 mutants.

• Epigenetics and aging