A key role of the EMC complex for mitochondrial respiration and quiescence in fission yeasts
In eukaryotes, oxygen consumption is mainly driven by the respiratory activity of mitochondria, which generates most of the cellular energy that sustains life. This parameter provides direct information about mitochondrial activity of all aerobic biological systems. Using the Seahorse analyzer instrument, we show here that deletion of the oca3/emc2 gene (oca3{Delta}) encoding the Emc2 subunit of the ER membrane complex (EMC), a conserved chaperone/insertase which aids membrane protein biogenesis in the ER, severely affects oxygen consumption rates and quiescence survival in Schizosaccharomyces pombe yeast cells. Remarkably, the respiratory defects of the oca3{Delta} mutation (EMC dysfunction) is rescued synergistically by the disruption of ergosterol biosynthesis (erg5{Delta}) and the action of the membrane fluidizing agent tween 20, suggesting a direct role of membrane fluidity and sterols composition in mitochondrial respiration in the fission yeast.