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Media type:
E-Article
Title:
Deactivation blocks proton pathways in the mitochondrial complex I
Contributor:
Röpke, Michael;
Riepl, Daniel;
Saura, Patricia;
Di Luca, Andrea;
Mühlbauer, Max E.;
Jussupow, Alexander;
Gamiz-Hernandez, Ana P.;
Kaila, Ville R. I.
imprint:
Proceedings of the National Academy of Sciences, 2021
Published in:Proceedings of the National Academy of Sciences
Language:
English
DOI:
10.1073/pnas.2019498118
ISSN:
0027-8424;
1091-6490
Origination:
Footnote:
Description:
<jats:title>Significance</jats:title>
<jats:p>The electron transport chain of mitochondria is initiated by the respiratory complex I that converts chemical energy into a proton motive force to power synthesis of adenosine triphosphate. On a chemical level, complex I catalyzes elementary electron and proton transfer processes that couple across large molecular distances of >300 Å. However, under low oxygen concentrations, the respiratory chain operates in reverse mode and produces harmful reactive oxygen species. To avoid cell damage, the mitochondrial complex I transitions into a deactive state that inhibits turnover by molecular principles that remain elusive. By combining large-scale molecular simulations with cryo-electron microscopy data, we show here that complex I deactivation blocks the communication between proton pumping and redox modules by conformational and hydration changes.</jats:p>