Date : Le mardi 5 septembre 2017
Heure : De 12 h 00 à 13 h 00
Type : Conférences et séminaires
Public : Tout public
Lieu : Hôpital et Centre d’hébergement D’Youville 1036, rue Belvédère Sud Auditorium, local 2458 à SherbrookeDisponible en visioconférence (réservez tôt)
Coût : Aucun frais
Description : Reactive Oxygen Species (ROS) are thought to be a primary factor in ageing and age-related diseases. However, ROS participate, as cellular messengers, in essential physiological processes including cell differentiation, the immune response and cancer progression. The participation of ROS in physiological processes is associated with specific ROS signals generated at or by specific respiratory complexes in response to precise stimuli. Conversely, in ageing and age-associated pathologies it is associated with the production of a general unspecific ROS. My laboratory has developed technology to precisely manipulate the generation of ROS in vivo. This technology coupled with state-of-the-art imaging and quantification methods, greatly increases the resolution of ROS measurements allowing the identification of which complex(es) is generating ROS. For example, inducing site specific ROS signalling via stimulation of reverse electron transport (RET) at CI protects mitochondrial function and extends lifespan in Drosophila. Conversely, inhibition of this RET-ROS signalling pathway causes the accumulation of respiratory deficient mitochondria and shortens lifespan. Importantly, the same RET-ROS pathway has been shown to be involved in multiple pathological and physiological situations such as ischemia-reperfusion, sensing of oxygen levels at the carotid body and reprogramming of macrophages in response to bacterial infection). Existing data indicates the co existence of two types of ROS. Firstly, ROS associated with macromolecular damage via oxidative distress (i.e. oxidative stress beyond physiological limits) that have been extensively studied and characterized. Secondly, ROS involved in site specific ROS signalling such as RET-ROS. During my talk, I will discuss the role of RET-ROS as a major sensor of mitochondrial status and how this new signalling pathway participates in cellular signalling and can contribute to accelerate ageing and age-related diseases when deregulated.
I obtained a PhD in Biology from the Complutense University of Madrid in 2006. During my PhD studies at laboratory of Prof Gustavo Barja, I studied how mitochondrial ROS levels are altered in response to changes in the diet (Sanz A and col. FASEB J. 2006). I did my postdoc, supported by an EMBO Long Term Fellowship, in the laboratory of Prof Howy Jacobs in Finland, where I generated Drosophila models to manipulate mitochondrial ROS levels in vivo (Fernandez-Ayala and col. 2009. Cell Metabolism & Sanz and col. PNAS. 2010). In 2011, I started my own laboratory, supported by an ERC Starting Grant, to study the role of mitochondria in ageing. Since 2014, my laboratory is based in Newcastle (UK) where I am a Research Fellow of Newcastle University supported by BBSRC, MRC and Wellcome Trust. Here, I am studying how mitochondrial ROS participate in ageing and age related diseases. Recently, my laboratory has described how site specific ROS signalling can protect mitochondrial function and extend lifespan (Scialo and col. Cell Metabolism. 2016).