BioMediTech, ARVO Building, Yellow Auditorium (F0025), Address: Lääkärinkatu 1
Free entrance, no registration needed. Presentations will last 20‐25 minutes + 5‐10 min for questions.
13:00‐13:30 Helen Cooper (Åbo University, Finland): “Cellular Landscapes”
- Helen will present images of the molecular architecture of cells, and discuss how structural organization relates to function in and outside mitochondria.
13‐30‐14:00 Joachim Gerholt (University of Tartu, Estonia): “Moving parts in a moving system – mitochondrial DNA maintenance within the mitochondrial network”
- Faithful mitochondrial DNA maintenance is important to support mitochondrial function. Joachim will present you the steps he undertook to understand how our knowledge of mitochondrial DNA replication relates to the dynamics of the mitochondrial network.
14:00‐14:30 Steffi Goffart (University of Joensuu, Finland): “Topoisomerase functions in mitochondria”
- Topoisomerase enzymes are essential for transcription, replication and repair of any genome, but little is known about the four topoisomerases existing in mitochondria. Steffi will present the functions of these enzymes and the mitochondrial off‐target effects of the topoisomerase inhibitors commonly used as antibiotics and cytostatins.
14:30-14:45 Coffee break…
14:45‐15:15 Reetta Hinttala (University of Oulu, Finland): “NHLRC2 Mutations Cause Fatal Fibrosis, Neurodegeneration and Leptomeningeal Angiomatosis (FINLA)”
- Reetta will describe the first pathogenic mutations in NHLRC2 causing a novel disease called FINLA. Using knockout mouse model and patient data she will demonstrate that NHLRC2 has an essential role in early development and multiorgan homeostasis.
15:15‐15:45 Jukka Kallijärvi (University of Helsinki, Finland): “Interventions in mouse model of GRACILE syndrome, a Finnish respiratory chain complex III deficiency disorder”
- GRACILE syndrome is a lethal fetal‐onset respiratory chain complex III deficiency manifesting mainly as hepatopathy. Jukka will give an overview of the Bcs1l knock‐in mouse model, the only viable CIII deficiency model, and some of the dietary and pharmacological interventions that his group has performed using this model.