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A01 - Proteolytic control of mitochondrial dynamics and cell survival by OMA1

The project aims to define the role of the stress-activated peptidase OMA1 in the regulation of mitochondrial dynamics and function in response to stress and different metabolic demands. The project combines multiple proteomic approaches and experiments in cultured cells with in vivo approaches in mouse to unravel how OMA1 regulates the stress response of mitochondria and cell survival and to uncover novel functions of OMA1 within mitochondria.

Latest publications
Sprenger, H.G., Wani, G., Hesseling, A., König, T., Patron, M., MacVicar, T., Ahola, S., Wai, T., Barth, E., Rugarli, E.I., Bergami, M., Langer, T. (2018). Loss of the mitochondrial i‐AAA protease YME1L leads to ocular dysfunction and spinal axonopathy. EMBO Mol Med. pii: e9288. doi: 10.15252/emmm.201809288. [Epub ahead of print]

Saita, S., Nolte, H., Fiedler, K.U., Kashkar, H., Venne, A.S., Zahedi, R.P., Krüger, M., and Langer, T. (2017). PARL mediates Smac proteolytic maturation in mitochondria to promote apoptosis. Nat Cell Biol. 19, 318-328.

Wang, S., Jacquemyn, J., Murru, S., Martinelli, P., Barth, E., Langer, T., Niessen, C.M., and Rugarli, E.I. (2016). The mitochondrial m-AAA protease prevents demyelination and hair greying. PLoS Genet 12, e1006463.

Wai, T., García-Prieto, J., Baker, M.J., Merkwirth, C., Benit, P., Rustin, P., Rupérez, F.J., Barbas, C., Ibanez, B., and Langer, T. (2015). Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice. Science, 350.