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Mitochondrial Translation Efficiency Controls Cytoplasmic Protein Homeostasis

Journal article
Authors T. Suhm
J. M. Kaimal
H. Dawitz
C. Peselj
A. E. Masser
Sarah Hanzén
M. Ambrozic
A. Smialowska
M. L. Bjorck
P. Brzezinski
Thomas Nyström
S. Buttner
C. Andreasson
M. Ott
Published in Cell Metabolism
Volume 27
Issue 6
Pages 1309-1322.e6
ISSN 1550-4131
Publication year 2018
Published at Institute of Biomedicine
Pages 1309-1322.e6
Language en
Keywords chronological life-span, shock transcription factor, saccharomyces-cerevisiae, misfolded proteins, gene-expression, quality-control, yeast, ribosome, activation, mechanism, Cell Biology, Endocrinology & Metabolism
Subject categories Cell Biology, Endocrinology and Diabetes


Cellular proteostasis ismaintained via the coordinated synthesis, maintenance, and breakdown of proteins in the cytosol and organelles. While biogenesis of the mitochondrial membrane complexes that execute oxidative phosphorylation depends on cytoplasmic translation, it is unknown how translation within mitochondria impacts cytoplasmic proteostasis and nuclear gene expression. Here we have analyzed the effects of mutations in the highly conserved accuracy center of the yeast mitoribosome. Decreased accuracy of mitochondrial translation shortened chronological lifespan, impaired management of cytosolic protein aggregates, and elicited a general transcriptional stress response. In striking contrast, increased accuracy extended lifespan, improved cytosolic aggregate clearance, and suppressed a normally stress-induced, Msn2/4-dependent interor-ganellar proteostasis transcription program (IPTP) that regulates genes important for mitochondrial proteostasis. Collectively, the data demonstrate that cytosolic protein homeostasis and nuclear stress signaling are controlled by mitochondrial translation efficiency in an inter-connected organelle quality control network that determines cellular lifespan.

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