Angela Giangrande

Angela Giangrande trained in Italy as an undergraduate and obtained her PhD in Strasbourg, where she developed her interests in transcriptional regulation and in the Drosophila melanogaster genetic model. After an EMBO postdoctoral fellowship in the USA, she returned to Strasbourg where she set up her group at the IGBMC, directed by Prof Chambon. She has characterized Drosophila neural stem cells and the glial fate determinant, Glide/Gcm, an evolutionarily conserved transcription factor. As their vertebrate counterpart, Drosophila glia control neuronal development/function and act as vertebrate microglia, macrophages that reshape the nervous system during development and in pathological conditions. Defective glia and microglia are at the basis of severe neural pathologies. The current projects aim at understanding the role of Glide/Gcm and its conserved pathway in the nervous system.
Drosophila provides a unique opportunity to study human diseases and Giangrande’s team has also contributed with two models, Fragile X Mental Retardation and Retinitis Pigmentosa.
As a Directeur de Recherche CNRS, Angela Giangrande has been awarded and coordinated several national and international grants (HFSP, EEC, ANR, FRM, ARC, LIGUE, AFM). She has also been awarded the Franco-Taiwanese International Prize by the Académie des Sciences (2009).

Post-doc: Yoshihiro Yuasa

Immune, degenerative and inflammatory diseases of the nervous system represent a heavy burden for our societies, and understanding the pathways controlling the formation and the integrity of the nervous system remains one of the most exciting issues in the area of neurobiology.
Recent studies indicate that microglia, cells of immune origin, play a key role in those diseases. These cells constitute the resident macrophages of the vertebrate nervous system and are thus crucial for the first response to damage, however, the molecular mechanisms controlling their development and activity are still poorly understood.
Drosophila provides a powerful genetic model to explore conserved pathways and the functional equivalent of microglia are the glial cells. In flies, this cell population as well as the macrophages circulating outside the nervous system, depends on a single gene called Glide/Gcm. When this gene is absent, gliogenesis and hematopoiesis are defective.
This gene is evolutionarily conserved and our data suggest that the ortholog genes have a similar conserved key role in the vertebrate immune system, including humans.
We are now testing the hypothesis that this gene is necessary for the development/function of microglia in mice, and that its lack has an impact on the immune response. In the long run, a better understanding of the function of Glide/Gcm genes may help identifying novel therapeutical targets for severe human pathologies, such as multiple sclerosis, neurodegeneration and inflammatory diseases.