New findings in mitochondrial biology thoroughly change the idea scientists had for 20 years on the role and importance of the protein MTERF1. For the first time, Max Planck researcher Mügen Terzioglu investigated in vivo what was up to now only explored in cell culture. Using the mouse as a model organism, she made a surprising discovery:
MTERF1 does after all not play the key role in mitochondrial transcription and translation that was hitherto ascribed to it. Terzioglu’s findings will change the way we look at the regulation of mitochondrial function in the cell.With her study, the young researcher demonstrates the way science often works: Long-standing research findings might be overthrown by surprising new insights, thus necessitating future projects with regard to related questions to take on a whole new direction. Mügen Terzioglu is a researcher in the department „Mitochondrial Biology“, headed by Director Nils-Göran Larsson at the Max Planck Institute (MPI) for Biology of Ageing in Cologne. She carried out her project with an international team of scientists at the MPI and at the Karolinska Institute in Stockholm.
“Up to now, the role of MTERF1 was only investigated in vitro, using cell culture. And for two decades, this protein was thought to play a crucial role in the regulation of transcription, eventually acting as a key regulator for mitochondrial protein synthesis in mammals“, explains Mügen Terzioglu. “However, by engineering an appropriate mouse model for the first time, we have now learned that this is not the case. That was actually quite a surprise to us.“ It also illustrates the fact that in vitro systems like cell culture can only to a certain extent represent a natural physiological condition. Consequently, the insights gained in vitro must always be verified in vivo.
Mügen Terzioglu’s findings will change the way we look at proteins and understand their roles in the cell. In particular, a new perspective opens up to better understand the regulation in mitochondrial transcription and translation as well as the stability of the mitochondrial transcripts and their metabolism.Original publication:
Sabine Dzuck | Max-Planck-Institut
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