Quantitative proteomics identifies redox switches for global translation modulation by mitochondrially produced reactive oxygen species

Ulrike Topf, Ida Suppanz, Lukasz Samluk, Lidia Wrobel, Alexander Böser, Paulina Sakowska, Bettina Knapp, Martyna K. Pietrzyk, Agnieszka Chacinska () and Bettina Warscheid ()
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Ulrike Topf: International Institute of Molecular and Cell Biology
Ida Suppanz: University of Freiburg
Lukasz Samluk: International Institute of Molecular and Cell Biology
Lidia Wrobel: International Institute of Molecular and Cell Biology
Alexander Böser: University of Freiburg
Paulina Sakowska: International Institute of Molecular and Cell Biology
Bettina Knapp: University of Freiburg
Martyna K. Pietrzyk: International Institute of Molecular and Cell Biology
Agnieszka Chacinska: International Institute of Molecular and Cell Biology
Bettina Warscheid: University of Freiburg

Nature Communications, 2018, vol. 9, issue 1, 1-17

Abstract: Abstract The generation of reactive oxygen species (ROS) is inevitably linked to life. However, the precise role of ROS in signalling and specific targets is largely unknown. We perform a global proteomic analysis to delineate the yeast redoxome to a depth of more than 4,300 unique cysteine residues in over 2,200 proteins. Mapping of redox-active thiols in proteins exposed to exogenous or endogenous mitochondria-derived oxidative stress reveals ROS-sensitive sites in several components of the translation apparatus. Mitochondria are the major source of cellular ROS. We demonstrate that increased levels of intracellular ROS caused by dysfunctional mitochondria serve as a signal to attenuate global protein synthesis. Hence, we propose a universal mechanism that controls protein synthesis by inducing reversible changes in the translation machinery upon modulating the redox status of proteins involved in translation. This crosstalk between mitochondria and protein synthesis may have an important contribution to pathologies caused by dysfunctional mitochondria.

Date: 2018
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DOI: 10.1038/s41467-017-02694-8

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