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 Home / About Us > Dr Robert A. Screaton

Contact info

Dr Robert A. Screaton
Sunnybrook Research Institute
2075, Bayview Avenue - Room M7 617
Toronto, ON M4N 3M5

E-mail: [email protected]

Link to Screaton Lab webpage


Research keywords

  • Pancreatic β cell
  • Islet
  • LKB1
  • AMPK family
  • Mitochondria
  • Cell-based screening
  • Imaging
  • Kinases
  • Genome-wide RNA interference


Robert A. Screaton, PhD
Associate Professor of Biochemistry
Canada Research Chair In Apoptotic Signaling

Biographical Sketch

Robert Screaton received his undergraduate and graduate training at McGill University in Montreal, Canada (1998), and pursued post-doctoral studies at the Burnham Institute (1999-2002) and the Salk Institute (2002-2005) in San Diego, California. Dr Screaton joined the Children's Hospital of Eastern Ontario Research Institute and the University of Ottawa in July 2005 where he is now Scientist and Assistant Professor. Dr Screaton is also the co-director of the CHEO-RI robotic cell based screening facility. He is the recipient of awards such as the Canada Research Chair In Apoptotic Signaling, Tier II (2006-2011, renewed 2011-2016) and Ontario Early Researcher Award (2006-2011). He has also recently received the CHEO Research Institute's Outstanding New Investigator Award (2009) and the University of Ottawa Faculty of Medicine's Young Professor Award (2009).

Click here for PubMed listing

Research Interests

Islet Biology
Current work in the lab is directed towards understanding how insulin-producing β cells respond to glucose and cAMP signals and to understand the signaling machinery that regulates β cell proliferation and regeneration. In this regard, we focus on the role of LKB1-AMPK signaling pathway and the CREB coactivator CRTC2. To identify novel gene products and signal transduction mechanisms that are involved in β cell biology, we employ biochemical, cell biological, proteomic and functional genomic approaches, and generate animal models to test the role of these genes in islet function and glucose metabolism in vivo.

Protein phosphorylation regulates virtually all cellular events. Protein kinases and their target proteins control central cell behaviours as proliferation, cell growth, differentiation, innate immunity, cell survival and death, and are of central importance both to basic research and to disease treatment. Identifying kinase substrate pairs, critical nodes in signal transduction pathways, represents a major challenge for understanding how information transfer takes place within a cell. We have developed a kinase screening platform to permit identification of kinase substrate pairs, and used this to elucidate novel pathways involved in glucose sensing. We have also applied the approach to a wide range of biological processes, including mitochondrial dynamics, phagocytosis axon guidance, and stem cell determination.

Cell Based Screening
We employ a state-of-the art robotic cell based screening facility to perform functional genetic screens in mammalian cells to identify novel genes involved in cell function and survival. We are currently performing large scale imaging screens using siRNA technology to identify novel genes that govern the initiation stages of the mitochondrial cell death program, with a view to identifying novel targets for therapeutic intervention for diseases in which inappropriate cell death is a root cause.

Mitochondrial Dynamics
The mitochondrial network is exquisitely sensitive to extracellular signals. Mitochondria becomes hyperfused in response to stress and fragment during cell death. Mitochondrial morphology is largely governed by opposing fission and fusion processes controlled by GTPase molecular switches. However, in mammalian systems, only a few players are known to affect the delicate balance between fragmentation and elongation of the mitochondrial network. Altered mitochondrial dynamics is seen in various disease models ranging from multiple neurodegenerative diseases to diabetes. We are currently using high throughput, high-content screens to identify novel regulators of mitochondrial dynamics, and also evaluating the potential for modulating the network for cancer therapy.

Mitochondrial Integrity
Recent data indicates that mitochondria possess several independent pathways for quality control and integrity, including mitophagy, or autophagic recycling of damaged mitochondria. Parkin, an E3 ubiquitin ligase and a Parkinson's disease gene, appears to function as a sensor of mitochondrial integrity. We are using a high-throughput, robotic imaging screen to look upstream in this pathway to identify novel genes that control Parkin activity, which may affect its recruitment (i.e. damage sensing or its retention of mitochondria).

� Montreal Diabetes Research Center 2018
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