Mistargeted mitochondrial proteins activate a proteostatic response in the cytosol

Lidia Wrobel, Ulrike Topf, Piotr Bragoszewski, Sebastian Wiese, Malgorzata E. Sztolsztener, Silke Oeljeklaus, Aksana Varabyova, Maciej Lirski, Piotr Chroscicki, Seweryn Mroczek, Elzbieta Januszewicz, Andrzej Dziembowski, Marta Koblowska, Bettina Warscheid () and Agnieszka Chacinska ()
Additional contact information
Lidia Wrobel: International Institute of Molecular and Cell Biology
Ulrike Topf: International Institute of Molecular and Cell Biology
Piotr Bragoszewski: International Institute of Molecular and Cell Biology
Sebastian Wiese: Faculty of Biology and BIOSS Centre for Biological Signalling Studies, University of Freiburg
Malgorzata E. Sztolsztener: International Institute of Molecular and Cell Biology
Silke Oeljeklaus: Faculty of Biology and BIOSS Centre for Biological Signalling Studies, University of Freiburg
Aksana Varabyova: International Institute of Molecular and Cell Biology
Maciej Lirski: Institute of Biochemistry and Biophysics Polish Academy of Sciences
Piotr Chroscicki: International Institute of Molecular and Cell Biology
Seweryn Mroczek: Institute of Biochemistry and Biophysics Polish Academy of Sciences
Elzbieta Januszewicz: International Institute of Molecular and Cell Biology
Andrzej Dziembowski: Institute of Biochemistry and Biophysics Polish Academy of Sciences
Marta Koblowska: Institute of Biochemistry and Biophysics Polish Academy of Sciences
Bettina Warscheid: Faculty of Biology and BIOSS Centre for Biological Signalling Studies, University of Freiburg
Agnieszka Chacinska: International Institute of Molecular and Cell Biology

Nature, 2015, vol. 524, issue 7566, 485-488

Abstract: Mitochondrial dysfunction and cellular protein homeostasis failure are hallmarks of many diseases and age-associated pathologies; this study shows that the mitochondrial import defect of nuclear-encoded proteins triggers a cellular pathway, termed unfolded protein response activated by mistargeting of proteins (UPRam), that acts to minimize the stress caused by non-imported mitochondrial precursor proteins in order to sustain cellular protein homeostasis and organismal fitness.

Date: 2015
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DOI: 10.1038/nature14951

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