When mitochondrial function is compromised and the mitochondrial membrane potential (Δψm) falls below a threshold, the F1Fo-ATP synthase can reverse, hydrolysing ATP to pump protons out of the mitochondrial matrix. Although this activity can deplete ATP and precipitate cell death, it is limited by the mitochondrial protein IF1, an endogenous F1Fo-ATPase inhibitor. IF1, therefore, preserves ATP at the expense of Δψm. Despite a wealth of detailed knowledge on the biochemistry of the interaction of IF1 and the F1Fo-ATPase, little is known about its physiological activity. Emerging research suggests that IF1 has a wider ranging impact on mitochondrial structure and function than previously thought.
ASJC Scopus subject areas
- Molecular Biology