ROS-based lethality ofCaenorhabditis elegansmitochondrial electron transport mutants grown onEscherichia colisiderophore iron release mutants

Abstract

Caenorhabditis elegansconsumes bacteria, which can supply essential vitamins and cofactors, especially for mitochondrial functions that have a bacterial ancestry. Therefore, we screened the KeioEscherichia coliknockout library for mutations that induce theC. elegans hsp-6mitochondrial damage response gene, and identified 45E. colimutations that inducehsp-6::gfp. We tested whether any of theseE. colimutations that stress theC. elegansmitochondrion genetically interact withC. elegansmutations in mitochondrial functions. Surprisingly, 4E. colimutations that disrupt the import or removal of iron from the bacterial siderophore enterobactin were lethal in combination with a collection ofC. elegansmutations that disrupt particular iron–sulfur proteins of the electron transport chain. Bacterial mutations that fail to synthesize enterobactin are not synthetic lethal with theseC. elegansmitochondrial mutants; it is the enterobactin–iron complex that is lethal in combination with theC. elegansmitochondrial 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.