The "Laboratoire de Génétique et Biologie Cellulaire" (LGBC - EA 4589) is a laboratory of the University of Versailles Saint-Quentin-en-Yvelines (UVSQ) in partnership with the "Ecole Pratique des Hautes Etudes" (EPHE)
The LGBC is affiliated to the Doctoral School"des Génomes Aux Organismes".
Our main research interests concern on the one hand cell death regulation and modalities, and on the other hand, the events controlling cell behaviors at the interface between death and proliferation. Indeed, we have focused our research on the role of p53 and RB oncosuppressor proteins in the determinism of cell fate (survival, death, proliferation, differentiation). These proteins are well known cell cycle regulators that can exert pro-apoptotic or pro-survival effects depending on the context. We also focus on tissue homeostasis regulation after cell death has occurred. For this purpose we use mammalian cellular models and Drosophila.
We are currently developing three complementary axes of research:
- Interactions between growth factor signaling and cell death pathways are crucial events that determine cell fate. We study the interactions between the cell death pathway controlled by p53 and the survival pathway controlled by Fibroblast Growth Factor 1 (FGF1) as a model of intracrine/nuclear survival factors.
- RBF, which is the homologue of the RB protein in Drosophila, can exert pro- or anti-apoptotic activities depending on the proliferative status of the cell. RBF can also play a role in non-cell autonomous proliferation. We are now characterizing its functions in the control of apoptosis and tissue homeostasis.
- Among various possible stresses, oxidation and protein aggregation are prominent. We study cell death and compensatory mechanisms associated with the formation of mitochondrial or endoplasmic reticulum stresses in Drosophila.
In parallel, we develop collaborative projects in areas such as survival and death pathways, mitochondria and cell death, responses to stress (in particular genotoxic, oxidant and endoplasmic reticulum stresses).