Cytosolic, but not matrix, calcium is essential for adjustment of mitochondrial pyruvate supply.

ABSTRACT: Mitochondrial oxidative phosphorylation (OXPHOS) and cellular workload are tightly balanced by the key cellular regulator, calcium (Ca²⁺). Current models assume that cytosolic Ca²⁺ regulates workload and that mitochondrial Ca²⁺ uptake precedes activation of matrix dehydrogenases, thereby matching OXPHOS substrate supply to ATP demand. Surprisingly, knockout (KO) of the mitochondrial Ca²⁺ uniporter (MCU) in mice results in only minimal phenotypic changes and does not alter OXPHOS. This implies that adaptive activation of mitochondrial dehydrogenases by intramitochondrial Ca²⁺ cannot be the exclusive mechanism for OXPHOS control. We hypothesized that cytosolic Ca²⁺, but not mitochondrial matrix Ca²⁺, may adapt OXPHO

SUBMITTER: Szibor M 

PROVIDER: S-EPMC7135991 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature