You are here : LGBCenglishLGBCResearch topics
- Partager cette page :
- PDF version
Research topics
We develop four complementary axes of research:
"Sideroflexins, mitochondria and cell fate" axis:
Beyond its crucial involvement in energetic metabolism, the mitochondria have many other functions. They integrate cellular stresses and can decide if a cell must die or subsist. Mitochondrial dysfunctions or altered mitochondrial dynamics are observed in several diseases (neurodegenerative, cancers, mitochondrial diseases). Our projects focus on the molecular mechanisms whereby mitochondria influence cell fate. We are currently investigating the role of sideroflexins that are mitochondrial proteins of unknown functions.
"Mitochondrial stress and apoptosis" axis:
Rbf1, the homolog of the RB protein in Drosophila, can exert pro- or anti-apoptotic activities depending on the proliferative status of the cell. We are currently studying the way by which, during Rbf1-induced apoptosis, Debcl (proapoptotic Drosophila Bcl-2 family member), induces mitochondrial fragmentation by binding the pro-fission protein Drp1, which triggers the production of mitochondrial reactive oxygen species (ROS), thereby activating the JNK (c-Jun N-terminal kinases) pathway and cell death.
"Mitochondria and ER stress resolution" axis:
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.
"Human pathological mechanisms in Drosophila" axis
We also develop Drosophila models that mimic human pathological mechanisms. In particular, we are studying the activities of the HLA-B27 antigen, the main genetic predisposing factor for ankylosing spondylitis, and looking for factors enabling Mycobacterium abcessus to resist the immune response.
"Sideroflexins, mitochondria and cell fate" axis:
Beyond its crucial involvement in energetic metabolism, the mitochondria have many other functions. They integrate cellular stresses and can decide if a cell must die or subsist. Mitochondrial dysfunctions or altered mitochondrial dynamics are observed in several diseases (neurodegenerative, cancers, mitochondrial diseases). Our projects focus on the molecular mechanisms whereby mitochondria influence cell fate. We are currently investigating the role of sideroflexins that are mitochondrial proteins of unknown functions.
"Mitochondrial stress and apoptosis" axis:
Rbf1, the homolog of the RB protein in Drosophila, can exert pro- or anti-apoptotic activities depending on the proliferative status of the cell. We are currently studying the way by which, during Rbf1-induced apoptosis, Debcl (proapoptotic Drosophila Bcl-2 family member), induces mitochondrial fragmentation by binding the pro-fission protein Drp1, which triggers the production of mitochondrial reactive oxygen species (ROS), thereby activating the JNK (c-Jun N-terminal kinases) pathway and cell death.
"Mitochondria and ER stress resolution" axis:
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.
"Human pathological mechanisms in Drosophila" axis
We also develop Drosophila models that mimic human pathological mechanisms. In particular, we are studying the activities of the HLA-B27 antigen, the main genetic predisposing factor for ankylosing spondylitis, and looking for factors enabling Mycobacterium abcessus to resist the immune response.