The specific V-ATPase inhibitor concanatmycin A (concA) blocks VMA1 or VPH2 overexpression mutations ability to produce normal, tubular mitochondria. Treatment of young cells causes vacuolar acidity and loss of mitochondrial depolarization. Loss of ΔΨ is followed by mitochondrial fragmentation and aggregation that resembles mitochondrial phenotypes present in aged cells [23172144].
Comment on This Data Unit