Contact
Areas of expertise
Biography
Eeva-Liisa Eskelinen has a long track record in autophagy field, in particular, in elucidating the fine structure and membrane dynamics of autophagosome biogenesis using electron microscopy. She completed her PhD in 1993 at the University of Jyväskylä, Finland. After that, she worked as postdoctoral researcher in Göttingen, Germany and Helsinki, Finland. Then she moved to Dundee, Scotland, where she worked as an independent investigator (1999-2002). From Scotland she moved to Kiel, Germany and worked as a group leader at the department headed by professor Paul Saftig (2002-2005). In August 2005 she moved back to Finland and worked as a University Lecturer at the Department of Biosciences, University of Helsinki, until 2017. 1st of November 2017 she started as a Professor of medical cell biology at the Institute of Biomedicine, University of Turku, Finland.
Teaching
Eeva-Liisa Eskelinen is the responsible teacher of the course Cell Biology and Histology, aimed for first year students in medicine, dentistry and biomedicine. She is also teaching electron microscopy methods on the course Electron Microscopy in Biomedical Sciences, aimed for MSc students on Biomedical Imaging, and for PhD students interested in the topic.
Research
The small GTPase RAB24
We study the biological functions and molecular mechanisms of RAB24, a GTPase that we showed to function in the late phase of the macroautophagic pathway. Mutation in RAB24 causes hereditary ataxia in dogs. In addition, RAB24 was shown to be overexpressed in hepatocellular carcinoma, and the overexpression was further shown to facilitate the malignant phenotype of the cancer cells. RAB24 is also overexpressed in non-alcoholic fatty liver disease. We use cell and molecular biological and biochemical approaches in order to clarify the biological functions of RAB24, as well as the molecular mechanisms that mediate these functions.
Membrane dynamics in autophagy
Autophagy is a lysosomal degradation pathway for cytoplasmic material and organelles that maintains cellular homeostasis during nutrient deprivation and stress. Autophagy also contributes to the clearance of damaged organelles and aggregate-prone proteins, protection against metabolic stress and DNA damage, and even to longevity of the organism. Defective autophagy has been connected to many human diseases including cancer, myopathies, metabolic diseases, and neurodegenerative diseases.
We and others showed that autophagosomes form in a subcompartment of the endoplasmic reticulum. A flat membrane cistern called the phagophore emerges first, which then elongates and forms a double-membrane bound autophagosome. Autophagosomes acquire hydrolytic capacity by fusing with endosomes and lysosomes. The origin of autophagosome membranes is one of the longest lasting open questions in the field. We have addressed this question using three-dimensional electron microscopy, live-cell imaging and correlative light-electron microscopy.