Regulation of Mitochondrial Structure and Function by the F1Fo-ATPase Inhibitor Protein, IF1

Michelangelo Campanella, Edward Casswell, Stephanie Chong, Ziad Farah, Mariusz R. Wieckowski, Andrey Y. Abramov, Andrew Tinker, Michael R. Duchen

Research output: Contribution to journalArticlepeer-review

Abstract

When mitochondrial respiration is compromised, the F1Fo-ATP synthase reverses and consumes ATP, serving to maintain the mitochondrial membrane potential (Δψm). This process is mitigated by IF1. As little is known of the cell biology of IF1, we have investigated the functional consequences of varying IF1 expression. We report that, (1) during inhibition of respiration, IF1 conserves ATP at the expense of Δψm; (2) overexpression of IF1 is protective against ischemic injury; (3) relative IF1 expression level varies between tissues and cell types and dictates the response to inhibition of mitochondrial respiration; (4) the density of mitochondrial cristae is increased by IF1 overexpression and decreased by IF1 suppression; and (5) IF1 overexpression increases the formation of dimeric ATP synthase complexes and increases F1Fo-ATP synthase activity. Thus, IF1 regulates mitochondrial function and structure under both physiological and pathological conditions.

Original languageEnglish
Pages (from-to)13-25
Number of pages13
JournalCell Metabolism
Volume8
Issue number1
DOIs
Publication statusPublished - Jul 2 2008

Keywords

  • HUMDISEASE
  • PROTEINS

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Physiology

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