ROS-based lethality of mitochondrial electron transport mutants grown on siderophore iron release mutants.

consumes bacteria, which can supply essential vitamins and cofactors, especially for mitochondrial functions that have a bacterial ancestry. Therefore, we screened the Keio knockout library for mutations that induce the mitochondrial damage response gene, and identified 45 mutations that induce We tested whether any of these mutations that stress the mitochondrion genetically interact with mutations in mitochondrial functions. Surprisingly, 4 mutations that disrupt the import or removal of iron from the bacterial siderophore enterobactin were lethal in combination with a collection of mutations that disrupt particular iron-sulfur proteins of the electron transport chain. Bacterial mutations that fail to synthesize enterobactin are not synthetic lethal with these mitochondrial mutants; it is the enterobactin-iron complex that is lethal in combination with the mitochondrial mutations. Antioxidants suppress this inviability, suggesting that reactive oxygen species (ROS) are produced by the mutant mitochondria in combination with the bacterial enterobactin-iron complex.