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B01 - Oxidative stress signalling in lifespan regulation

Aleksandra Trifunovic
CECAD Forschungszentrum/Institut für Mitochondriale Erkrankungen und Alterung
Universitätsklinikum Köln

E-mail: aleksandra.trifunovic(at)uk-koeln.de
Phone: +49 - 221 / 478 84291
For more information and contact please visit the TRIFUNOVIC LAB.

Abstract
Increased ROS production has been detected in a number of long-lived mitochondrial mutants leading to the hypothesis that ROS may be a lifespan-promoting signal, which transduce inputs from the mitochondria to other compartments of the cell. However, molecular mechanisms and signalling steps behind this process are largely unknown. We recently identified a transcription factor that mediates a hormetic response to increased ROS triggering mitochondria-induced longevity. Based on these findings we aim to dissect ROS signalling initiated in mitochondria by analysing downstream and upstream factors through genetic screens and functional analysis of candidate proteins.

Latest publications
Seiferling, D., Szczepanowska, K., Becker, C., Senft, K., Hermans, S., Maiti, P., König, T., Kukat, A., Trifunovic, A. (2016). Loss of CLPP alleviates mitochondrial cardiomyopathy without affecting the mammalian UPRmt. EMBO Rep. 17, 953-964.

Guarás, A., Perales-Clemente, E., Calvo, E., Acín-Pérez, R., Loureiro-Lopez, M., Pujol, C., Martínez-Carrascoso, I., Nuñez, E., García-Marqués, F., Rodríguez-Hernández, M.A., Cortés, A., Diaz, F., Pérez-Martos, A., Moraes, C.T., Fernández-Silva, P., Trifunovic, A., Navas, P., Vazquez, J., Enríquez, J.A. (2016). The CoQH2/CoQ ratio serves as a sensor of respiratory chain efficiency. Cell Rep. 15, 197-209.

Szczepanowska, K., Maiti, P., Kukat, A., Hofsetz, E., Nolte, H., Senft, K., Becker, C., Ruzzenente, B., Hornig-Do, H.-T., Wibom, R., Wiesner, R.J., Krüger, M. and Trifunovic, A. (2016). CLPP coordinates mitoribosomal assembly through regulation of ERAL1 levels. EMBO J. 35, 2566-2583.