Gerardo Ferbeyre, M.D., Ph. D.
Département de biochimie & médecine moléculaire, Faculté de médecine
Chaire CIBC en recherche sur les causes du cancer du sein, Université de Montréal
Centre de recherche du Centre Hospitalier de l’Université de Montréal (CHUM)
Montréal, Québec, CANADA
Dr Gerardo Ferbeyre graduated with honors from the Medical School at the University of Havana, Cuba in 1987 and has a PhD in biochemistry from the University of Montreal in Canada where he studied ribozymes. He did postdoctoral training at Cold Spring Harbor Laboratory with Dr. Scott Lowe. There he established a link between the promyelocytic leukemia protein PML and oncogene-induced senescence and studied the role of p53 and p19ARF as mediators of cellular senescence. In October 2001, Dr Ferbeyre joined the Department of biochemistry of the University of Montreal to continue his scientific research on senescence. In 2018 he opened a new laboratory at the CRCHUM in Montreal to focus on translational research. Major contributions from his laboratory include the discovery that DNA damage signaling mediates senescence (Genes & Dev. 2007), the role of SOCS1 linking inflammation to p53 (Mol Cell 2009, Aging 2017, Cancer Res 2019), the role of proteasome dependent protein degradation as a key mediator of tumor suppression and senescence (Genes & Dev 2013), the mechanism of senescence induction by the anticancer drug palbociclib (Cancer Res 2016), the discovery of ribosome biogenesis defects associated to senescence (Nature Cell Biol 2018) and a new metabolic cycle that controls NAD metabolism (Mol Cell 2021).
Titre: Cellular senescence, aging and the nucleolus
Senescent cells accumulate with age and contribute to age-related pathology. Their elimination increase both life and health span. All senescent cells display alterations in the nucleolus and ribosome biogenesis. In addition, nucleolar alterations can be observed in multiple tissues from old organisms. It is not known whether these changes are causal to aging. We used a conditional knockdown system to inhibit ribosome biogenesis in living mice. Ribosome biogenesis defective (Rib-def) mice develop an accelerated aging phenotype and accumulation of senescent cells in multiple stem cell compartments. Our results link defective ribosome biogenesis to aging and propose Rib-def mice as a model to test anti-aging therapies.