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Fujikawa M.,JST ICORP ATP Synthesis Regulation Project | Fujikawa M.,Tokyo Medical and Dental University | Sugawara K.,JST ICORP ATP Synthesis Regulation Project | Sugawara K.,Japan Womens University | And 4 more authors.
FEBS Letters

Mitochondrial ATP synthase is a motor enzyme in which a central shaft rotates in the stator casings fixed with the peripheral stator stalk. When expression of d-subunit, a stator stalk component, was knocked-down, human cells could not form ATP synthase holocomplex and instead accumulated two subcomplexes, one containing a central rotor shaft plus catalytic subunits (F1-c-ring) and the other containing stator stalk components ("b-e-g" complex). F1-c-ring was also formed when expression of mitochondrial DNA-coded a-subunit and A6L was suppressed. Thus, the central rotor shaft and the stator stalk are formed separately and they assemble later. Similar assembly strategy has been known for ATP synthase of yeast and Escherichia coli and could be common to all organisms. © 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. Source

Fujikawa M.,JST ICORP ATP Synthesis Regulation Project | Fujikawa M.,Tokyo University of Science | Ohsakaya S.,Tokyo Institute of Technology | Sugawara K.,JST ICORP ATP Synthesis Regulation Project | And 3 more authors.
Genes to Cells

A 6.8-kDa proteolipid (called MLQ) is a hydrophobic mitochondrial protein with unknown function that is loosely associated with ATP synthase. Here, we show that MLQ-knockdown HeLa cells lose population of ATP synthase in mitochondria. This is not due to low transcription of subunit genes of ATP synthase because levels of mRNA for α- and β-subunits are unaffected by the knockdown. As a consequence, the knockdown cells show low mitochondrial ATP synthesis activity, grow slowly in the normal medium, and are vulnerable to glucose deprivation. Given that the expression of MLQ varies responding to cellular conditions, MLQ is a potential regulator of the mitochondrial ATP synthesis. © 2013 by the Molecular Biology Society of Japan and Wiley Publishing Asia Pty Ltd. Source

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