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Prof. Dr. Aleksandra Trifunovic

Principal Investigator, Institute for Genetics

Prof. Dr. Aleksandra Trifunovic
Principal Investigator, Institute for Genetics
Tel.  +49 221 478 842 91
aleksandra.trifunovic[at]uk-koeln.de

CECAD Research Center
Universität zu Köln
Joseph-Stelzmann-Str. 26
50931 Köln
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Aleksandra Trifunovic

Prof. Dr. Aleksandra Trifunovic and her research group are investigating mitochondrial stress responses and the cell’s corresponding adaptive reactions. By deciphering the signaling cascades, they are seeking to understand the pathomechanisms of mitochondrial diseases and develop new therapeutic approaches. The group has recently started collaborating with Khondrion, one of the first European companies aiming to develop drugs to treat mitochondrial diseases. Prof. Dr. Trifunovic’s group will focus on evaluating the therapeutic effects in model organisms.

Our research: The team led by Prof. Aleksandra Trifunovic is investigating the function of mitochondria in the development of disease and during aging. When mitochondria experience stress or when dysfunction occurs, they send signals to the cell nucleus, which launches different types of adaptive cell responses. Transcription factors are activated and stimulate the expression of specific sets of genes, whose products enable the cell to adapt to the changes. The scientists aim to understand this signaling cascade in detail.

Our successes: The group has successfully advanced research approaches that focus on the communication between mitochondria and other parts of the cell. Causative treatment for mitochondrial disease is not yet available. Since mitochondrial dysfunction affects metabolism in general, serious illness and early death can result. Recently, the group has shown that mitochondrial dysfunction is sensed independently of respiratory chain deficiency, questioning the current view on molecular mechanisms contributing to the development of mitochondrial diseases.

Our goals: The group’s main focus is on deciphering the precise signaling cascade of the pathogenic mechanisms leading to mitochondrial diseases, with the ultimate goal of identifying new therapeutic targets.

Our methods/techniques: The group mainly uses in vivo model systems, specifically the roundworm Caenorhabditis elegans and transgenic mice to tackle specific questions of mitochondrial pathophysiology. As one of the main aims is to understand the consequences of energy depletion in cells and the organism as a whole, many different bioenergy techniques and approaches are used.

Figures
Figure 1
Figure 2

Figure 1: Mitochondrial dysfunction causes progressive neuronal loss. Hippocampal area of brains from control (L/L) and aspartyl-tRNA synthentase, forebrain neuron-deficient mice - Dars2 L/L; +/CamKII-cre (L/L, cre) stained by Nissl staining, used to highlight important structural features of different types of neurons. Clear sign of progressive neuronal degeneration are visible in mitochondrial mutant.

Figure 2: Histological analysis of mitochondrial dysfunction. Cytochrome c oxidase (COX) activity (brown) highlights integrity of mitochondrial function while succinate dehydrogenase (SDH) activity (blue) increases in respiratory chain deficient cells. In this figure, cross-sections of hearts of DARS2 deficient-mice (a gene essential for mitochondrial translation), show a strong mitochondrial dysfunction (left side). This effect can be partially reversed, if these mice are depleted in addition of CLPP, a mitochondrial matrix protease (right side).

EXTERNAL Cooperations
  • PD Dr. S. Meiners, Helmholtz Zentrum, Munich, DE
  • Prof. Dr. M. Ott, Stockholm University, SE
  • Prof. Dr. A. Suomalainen, University of Helsinki, FI
  • Prof. Dr. S. Werner, ETH, Zürich, CH