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Regulation of mitochondrial protein import by cytosolic kinases |
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| Authors: | Schmidt Oliver Harbauer Angelika B Rao Sanjana Eyrich Beate Zahedi René P Stojanovski Diana Schönfisch Birgit Guiard Bernard Sickmann Albert Pfanner Nikolaus Meisinger Chris |
| Institution: | 1 Institut für Biochemie und Molekularbiologie, ZBMZ, Universität Freiburg, 79104 Freiburg, Germany 2 BIOSS Centre for Biological Signalling Studies, Universität Freiburg, 79104 Freiburg, Germany 3 Fakultät für Biologie, Universität Freiburg, 79104 Freiburg, Germany 4 Spemann Graduate School of Biology and Medicine, Universität Freiburg, 79104 Freiburg, Germany 5 Leibniz-Institut für Analytische Wissenschaften-ISAS-e.V., 44139 Dortmund, Germany 6 Department of Biochemistry, La Trobe University, 3086 Melbourne, Australia 7 Centre de Génétique Moléculaire, CNRS, 91190 Gif-sur-Yvette, France 8 Medizinisches Proteom-Center, Ruhr-Universität Bochum, 44801 Bochum, Germany 9 Department of Chemistry and Biochemistry, University of Bern, 3012 Bern, Switzerland |
| Abstract: | Mitochondria import a large number of nuclear-encoded proteins via membrane-bound transport machineries; however, little is known about regulation of the preprotein translocases. We report that the main protein entry gate of mitochondria, the translocase of the outer membrane (TOM complex), is phosphorylated by cytosolic kinases-in particular, casein kinase 2 (CK2) and protein kinase A (PKA). CK2 promotes biogenesis of the TOM complex by phosphorylation of two key components, the receptor Tom22 and the import protein Mim1, which in turn are required for import of further Tom proteins. Inactivation of CK2 decreases the levels of the TOM complex and thus mitochondrial protein import. PKA phosphorylates Tom70 under nonrespiring conditions, thereby inhibiting its receptor activity and the import of mitochondrial metabolite carriers. We conclude that cytosolic kinases exert stimulatory and inhibitory effects on biogenesis and function of the TOM complex and thus regulate protein import into mitochondria. |
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