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Interaction between AIF and CHCHD4 Regulates Respiratory Chain Biogenesis

Journal article
Authors Emilie Hangen
Olivier Féraud
Sylvie Lachkar
Haiwei Mou
Nunzianna Doti
Gian Maria Fimia
Ngoc-Vy Lam
Changlian Zhu
Isabelle Godin
Kevin Muller
Afroditi Chatzi
Esther Nuebel
Fabiola Ciccosanti
Stéphane Flamant
Paule Bénit
Jean-Luc Perfettini
Allan Sauvat
Annelise Bennaceur-Griscelli
Karine Ser-Le Roux
Patrick Gonin
Kostas Tokatlidis
Pierre Rustin
Mauro Piacentini
Menotti Ruvo
Klas Blomgren
Guido Kroemer
Nazanine Modjtahedi
Published in Molecular cell
Volume 58
Issue 6
Pages 1001-1014
ISSN 1097-4164
Publication year 2015
Published at Institute of Neuroscience and Physiology
Institute of Clinical Sciences, Department of Pediatrics
Pages 1001-1014
Language en
Keywords Amino Acid Sequence, Animals, Apoptosis Inducing Factor, genetics, metabolism, Cell Line, Tumor, Electron Transport, genetics, Electron Transport Chain Complex Proteins, genetics, metabolism, Embryo, Mammalian, embryology, metabolism, Embryonic Development, genetics, Humans, Immunoblotting, Mice, Knockout, Mitochondria, genetics, metabolism, Mitochondrial Membrane Transport Proteins, genetics, metabolism, Molecular Sequence Data, Protein Binding, Protein Transport, genetics, RNA Interference, Time Factors
Subject categories Cell Biology


Apoptosis-inducing factor (AIF) is a mitochondrial flavoprotein that, beyond its apoptotic function, is required for the normal expression of major respiratory chain complexes. Here we identified an AIF-interacting protein, CHCHD4, which is the central component of a redox-sensitive mitochondrial intermembrane space import machinery. Depletion or hypomorphic mutation of AIF caused a downregulation of CHCHD4 protein by diminishing its mitochondrial import. CHCHD4 depletion sufficed to induce a respiratory defect that mimicked that observed in AIF-deficient cells. CHCHD4 levels could be restored in AIF-deficient cells by enforcing its AIF-independent mitochondrial localization. This modified CHCHD4 protein reestablished respiratory function in AIF-deficient cells and enabled AIF-deficient embryoid bodies to undergo cavitation, a process of programmed cell death required for embryonic morphogenesis. These findings explain how AIF contributes to the biogenesis of respiratory chain complexes, and they establish an unexpected link between the vital function of AIF and the propensity of cells to undergo apoptosis.

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