Supercomplex Assembly Determines Electron Flux in the Mitochondrial Electron Transport Chain

Esther Lapuente-Brun(Universidad de Zaragoza), Raquel Moreno‐Loshuertos(Universidad de Zaragoza), Rebeca Acín‐Pérez(Spanish National Centre for Cardiovascular Research), Ana Latorre(Spanish National Centre for Cardiovascular Research), Carmen Colás(Spanish National Centre for Cardiovascular Research), Eduardo Balsa(Spanish National Centre for Cardiovascular Research), Ester Perales‐Clemente(Spanish National Centre for Cardiovascular Research), Pedro M. Quirós(Universidad de Oviedo), Enrique Calvo(Universidad de Zaragoza), María Hernández(Centro Andaluz de Biología del Desarrollo), Plácido Navas(Centro Andaluz de Biología del Desarrollo), Raquel Cruz(Universidade de Santiago de Compostela), Ángel Carracedo(Universidade de Santiago de Compostela), Carlos López-Otı́n(Universidad de Oviedo), Acisclo Pérez‐Martos(Universidad de Zaragoza), Patricio Fernández‐Silva(Universidad de Zaragoza), Erika Fernández‐Vizarra(Instituto Aragonés de Ciencias de la Salud), José Antonio Enrı́quez(Universidad de Zaragoza)
Science
June 27, 2013
Cited by 818Open Access
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Abstract

The textbook description of mitochondrial respiratory complexes (RCs) views them as free-moving entities linked by the mobile carriers coenzyme Q (CoQ) and cytochrome c (cyt c). This model (known as the fluid model) is challenged by the proposal that all RCs except complex II can associate in supercomplexes (SCs). The proposed SCs are the respirasome (complexes I, III, and IV), complexes I and III, and complexes III and IV. The role of SCs is unclear, and their existence is debated. By genetic modulation of interactions between complexes I and III and III and IV, we show that these associations define dedicated CoQ and cyt c pools and that SC assembly is dynamic and organizes electron flux to optimize the use of available substrates.


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