In 2011, CFATG1 demonstrated that it was useful to arrange a gathering of members of the French-speaking scientific community around the theme of “autophagy”. CFATG2 has provided further confirmation of this. Thanks to your active participation during these two meetings, and your constructive feed-back, we can now look forward to CFATG3, which we hope will be attended by just as many enthusiastic participants. Between now and then, don’t forget that you can make your opinions known via the CFATG website (www.cfatg.org), where you will also find information about congresses, techniques and grants. CFATG membership is growing – may it continue to do so, so that we will be able to offer you a full “autophagy panoply” that provides you with everything you are looking for.
CFATG2 rewarded two posters of young researchers who present their work below :
Guillaume ROBERThas a Postdoctoral position in the team “Cell Death, Differentiation and Cancer” (Dr. Auberger – INSERM 1065), Centre Méditerranéen de Médecine Moléculaire, Nice, France.
“I am currently working in Dr. Auberger’s team in Nice on the mechanisms of resistance to conventional chemotherapies in hematologic malignancies and on new pharmacological approaches capable to eradicate these refractory tumors. The work presented at the 2012 CFATG meeting, showed the importance of an anti-apoptotic member of the Bcl-2 family (Bcl-B). We have established that this protein, already known to inhibit apoptotsis is also able to bind to Beclin-1, therefore impairing autophagic death consecutive to a metabolic stress.”
Johan ARNOLD, is in his first year of his Ph.D., in the UPR 9021 du CNRS “Immunologie et Chimie Thérapeutiques” – Institut de Biologie Moléculaire et Cellulaire, team of Dr. Sylviane Muller.
“Systemic lupus erythematous (SLE) is an autoimmune disease where lymphocytes of adaptive immunity among which T lymphocytes, are deregulated. Aside its general role as a cell protective mechanism under energetic stress, autophagy is an important contributor to lymphocyte survival and activation. We previously found that autophagy was deregulated in T cells from lupus-prone mice, but also during human SLE (Gros, Arnold et al., Autophagy 2012). This project aims at understanding the contribution of autophagy in the onset and progression of lupus. Mice deficient for autophagy in mature T cells, spontaneously developing lupus, will be generated. These mice will allow us to understand if autophagy plays a role during lupus in lymphocyte homeostasis and survival and consequently on the progression of the pathology. Identifying autophagy as a key mechanism in survival and hyperactivation of autoreactive lymphocytes during lupus may lead to new therapeutic options.”