Complex I and II are required for normal mitochondrial Ca2+ homeostasis

Publication date: Available online 13 July 2019Source: MitochondrionAuthor(s): Fabian Jaña, Galdo Bustos, José Rivas, Pablo Cruz, Felix Urra, Carla Basualto-Alarcón, Eduardo Sagredo, Melany Ríos, Alenka Lovy, Zhiwei Dong, Oscar Cerda, Muniswamy Madesh, César CárdenasAbstractCytosolic calcium (cCa2+) entry into mitochondria is facilitated by the mitochondrial membrane potential (ΔΨm), an electrochemical gradient generated by the electron transport chain (ETC). Is has been assumed that as long as mutations that affect the ETC do not affect the ΔΨm, the mitochondrial Ca2+ (mCa2+) homeostasis remains normal. We show that knockdown of NDUFAF3 and SDHB reduce ETC activity altering mCa2+ efflux and influx rates while ΔΨm remains intact. Shifting the equilibrium toward lower [Ca2+]m accumulation renders cells resistant to death. Our findings reveal an unexpected relationship between complex I and II with the mCa2+ homeostasis independent of ΔΨm.
Source: Mitochondrion - Category: Biochemistry Source Type: research